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Kidney disease following hematopoietic cell transplantation

Kidney disease following hematopoietic cell transplantation
Authors:
Sangeeta Hingorani, MD
Ala Abudayyeh, MD
Kenar D Jhaveri, MD
Section Editors:
Paul M Palevsky, MD
Robert S Negrin, MD
Deputy Editor:
Albert Q Lam, MD
Literature review current through: Sep 2023.
This topic last updated: Jul 24, 2023.

INTRODUCTION — Hematopoietic cell transplantation (HCT) offers a cure for many malignant and nonmalignant hematologic diseases, metabolic disorders, and immune deficiencies that were once incurable or fatal. However, it has been associated with the development of both acute and chronic kidney disease.

The term "hematopoietic cell transplantation" will be used throughout this topic as a general term to cover transplantation of progenitor cells from any source (eg, bone marrow, peripheral blood, cord blood). Otherwise, the source of such cells will be specified (eg, autologous peripheral blood progenitor cell transplantation). (See "Sources of hematopoietic stem cells".)

This topic will review the different forms of kidney disease that can occur among patients who have undergone HCT. Other complications related to HCT are discussed elsewhere:

●(See "Early complications of hematopoietic cell transplantation".)

●(See "Survival, quality of life, and late complications after hematopoietic cell transplantation in adults".)

TERMINOLOGY

●Autologous HCT – Autologous hematopoietic cell transplantation (HCT) refers to the use of a patient's own hematopoietic cells to reconstitute the bone marrow for treatment of a variety of cancers. Posttransplantation immunosuppressive therapy is not necessary in autologous HCT.

●Allogeneic HCT – Allogeneic HCT refers to the use of hematopoietic cells collected from a healthy person (not from the patients themselves) to reconstitute the bone marrow for treatment of a variety of hematologic malignancies and certain other hematologic disorders (eg, thalassemia, aplastic anemia). Posttransplantation immunosuppressive therapy is required, commonly with calcineurin inhibitors (CNIs).

●Myeloablative allogeneic HCT – Myeloablative allogeneic HCT utilizes high-dose conditioning regimens, frequently in combination with high-dose radiotherapy.

●Nonmyeloablative allogeneic HCT – Nonmyeloablative (or reduced-intensity) allogeneic HCT is generally used for patients who are older (>60 years) or have comorbid conditions. This procedure entails a lower dose of chemoradiotherapy and is frequently performed on an outpatient basis.

●Graft-versus-host disease (GVHD) – GVHD refers to multi-organ syndromes that can develop after allogeneic HCT. GVHD occurs when immune cells transplanted from a non-identical donor (graft) into the recipient (host) recognize the host cells as "foreign," thereby initiating a graft-versus-host reaction. GVHD may manifest as acute GVHD, chronic GVHD, or GVHD overlap syndrome. (See "Pathogenesis of graft-versus-host disease (GVHD)", section on 'Overview of GVHD'.)

●T cell-depleted (TCD) allogeneic HCT – TCD HCT refers to the use of a "megadose" of TCD hematopoietic stem cells. No posttransplantation immunosuppressive therapy to prevent GVHD is required.

ACUTE KIDNEY INJURY

Incidence and risk factors — Acute kidney injury (AKI) is a common complication after hematopoietic cell transplantation (HCT). In a systematic review of 36 cohort studies including 5144 patients that underwent HCT, the pooled estimated incidence of AKI and severe (stage 3) AKI were 55 and 8 percent, respectively, and the pooled estimated incidence of AKI requiring kidney replacement therapy was 7 percent [1]. Similar findings were reported in a large, single-center analysis of 616 patients undergoing allogeneic HCT between 2014 and 2017, which found a cumulative incidence of AKI and stage 3 AKI of 65 and 10 percent, respectively [2]. The risk of AKI depends upon the type of HCT performed (allogeneic versus autologous) and the conditioning regimen (myeloablative versus nonmyeloablative) used prior to the transplant (table 1). In general, allogeneic HCT is associated with a higher risk of AKI than autologous HCT, and myeloablative conditioning regimens are associated with a higher risk compared with nonmyeloablative regimens [1,3-5]. The highest risk of AKI is seen with myeloablative allogeneic HCT. The risk of AKI appears to be lower among patients undergoing T cell-depleted (TCD) allogeneic HCT who do not require posttransplantation immunosuppression [2].

Other risk factors for AKI in HCT recipients include volume depletion, sepsis, calcineurin inhibitor (CNI) use, prior exposure to nephrotoxic medications, preexisting chronic kidney disease (CKD), total body irradiation, and acute graft-versus-host disease (GVHD) (table 2).

Most cases of AKI develop 10 to 30 days after HCT and are diagnosed within the first 60 days after HCT [6-9].

Causes of AKI — The most common causes of acute kidney jury (AKI) after HCT (table 2) are prerenal disease, acute tubular necrosis, toxicity from medications (such as CNIs and antibiotics), hepatic sinusoidal obstruction syndrome (SOS), thrombotic microangiopathy, and viral infections (such as BK polyomavirus [BKPyV], adenovirus, and cytomegalovirus) [6-11]. Cytokine release syndrome is another cause of AKI among recipients of an HLA-haploidentical HCT [12,13]. Less frequent causes of AKI include tumor lysis syndrome and acute engraftment syndrome. In addition, AKI after HCT may result from more than one of these etiologies.

General causes — Many of the common causes of AKI among patients undergoing HCT are similar to those among the general population, including the following:

●Prerenal disease – Prerenal disease is common among patients undergoing HCT, particularly in the early posttransplantation period, and often results from volume depletion (due to vomiting or diarrhea). Patients undergoing HCT may also develop prerenal disease due to third-spacing of intravascular fluid into the interstitium in the setting of post-HCT capillary leak syndrome [14]. (See "Etiology and diagnosis of prerenal disease and acute tubular necrosis in acute kidney injury in adults".)

●Acute tubular necrosis – Acute tubular necrosis is typically seen during the period of pancytopenia in septic patients who may also be treated with one or more nephrotoxins, including amphotericin B (both liposomal and conventional), aminoglycosides, vancomycin, piperacillin-tazobactam, foscarnet, and cidofovir.

●Medication toxicity – CNIs, which are commonly administered after allogeneic HCT to prevent GVHD, may contribute to AKI after HCT. CNIs can cause AKI by means of renal vasoconstriction with subsequent prerenal injury, tubular toxicity, or kidney endothelial damage and thrombotic microangiopathy. However, some studies have questioned the association between the use of CNIs and the development of AKI after HCT [7,15-18]. A temporary reduction in dose or cessation of therapy may be indicated if AKI occurs. Frequent monitoring of the plasma creatinine concentration and CNI levels, with dose adjustments for rising creatinine values, is also helpful. (See "Cyclosporine and tacrolimus nephrotoxicity".)

Transplant-specific causes — A number of causes of AKI are unique to patients undergoing HCT:

●Hepatic sinusoidal obstruction syndrome – Hepatic SOS, previously known as hepatic veno-occlusive disease, is a potentially life-threatening complication that develops in up to 15 percent of adults who undergo HCT. This disorder is caused by chemoradiation-induced hepatic sinusoidal endothelial cell injury, which results in sinusoidal thrombosis and obstruction and portal hypertension. Patients typically present with tender hepatomegaly, fluid retention, weight gain, jaundice, and hyperbilirubinemia. AKI develops in approximately one-half of patients with SOS and is clinically indistinguishable from hepatorenal syndrome. Many cases are mild and managed with supportive care. The clinical presentation, diagnosis, and treatment of SOS are discussed in more detail separately. (See "Hepatic sinusoidal obstruction syndrome (veno-occlusive disease) in adults" and "Hepatic sinusoidal obstruction syndrome (veno-occlusive disease) in children".)

●Thrombotic microangiopathy – Transplant-associated thrombotic microangiopathy (TA-TMA) can present with AKI after HCT. The majority of cases of TA-TMA present within the first 100 days after transplantation. TA-TMA is also a common cause of CKD in this patient population and is discussed in more detail elsewhere in this topic. (See 'Thrombotic microangiopathy' below.)

●Viral infections – Viruses, such as adenovirus and BKPyV, can cause AKI in patients undergoing HCT. Adenovirus and BKPyV infections can cause tubulointerstitial nephritis [19] or ureteral obstruction secondary to hemorrhagic cystitis with resultant hydronephrosis [20]. BKPyV-associated nephropathy, which is more commonly seen in kidney transplant recipients, has also been reported in patients after HCT [21]. Treatment of these infections with cidofovir may also cause AKI. (See "Pathogenesis, epidemiology, and clinical manifestations of adenovirus infection", section on 'Genitourinary tract' and "Kidney transplantation in adults: BK polyomavirus-associated nephropathy", section on 'BKPyV-associated nephropathy (BKPyVAN)'.)

●Engraftment syndrome – Engraftment syndrome is a complication of HCT that commonly presents with fever, capillary leak, pulmonary edema, rash, and organ dysfunction. As this disorder is characterized by a cytokine storm, it can lead to intravascular volume depletion and AKI due to fluid shifts. (See "Pulmonary complications after allogeneic hematopoietic cell transplantation: Causes", section on 'Engraftment syndrome'.)

●Cytokine release syndrome – Recipients of an HLA-haploidentical peripheral blood HCT are at risk for developing a form of cytokine release syndrome (also known as haplostorm) in the first two weeks posttransplant [12,13]. Between 8 and 13 percent of such patients may develop AKI due to hemodynamic insults caused by the cytokine release syndrome [12,13]. (See "Cytokine release syndrome (CRS)".)

Evaluation of AKI — The evaluation of acute kidney injury (AKI) among patients who have undergone HCT is similar to that for the general population and includes a thorough history and physical examination, examination of the urinalysis and sediment and urine albumin-to-creatinine ratio, and imaging of the kidneys (algorithm 1). In addition, the evaluation should include an assessment for transplant-specific causes of AKI (see 'Transplant-specific causes' above), including the following:

●Complete blood count and platelet count

●Review of the peripheral blood smear for schistocytes

●Measurement of blood tacrolimus (or cyclosporine) concentration (in patients receiving these agents)

●Serum markers of hemolysis, including lactate dehydrogenase (LDH) and haptoglobin

●Measurement of blood adenovirus and BKPyV viral loads

In patients with AKI of unclear etiology, despite the evaluation described above, a kidney biopsy may be helpful to establish the diagnosis. Marked thrombocytopenia, which is common in patients after HCT, may increase the risk of bleeding after biopsy. However, with careful planning and platelet transfusion, a kidney biopsy can be performed safely if indicated. (See "The kidney biopsy", section on 'Thrombocytopenia'.)

Comprehensive discussions of the general approach to the evaluation of AKI are presented separately:

●(See "Evaluation of acute kidney injury among hospitalized adult patients".)

●(See "Diagnostic approach to adult patients with subacute kidney injury in an outpatient setting".)

●(See "Acute kidney injury in children: Clinical features, etiology, evaluation, and diagnosis".)

Management of AKI — In general, the overall management of acute kidney injury (AKI) among patients who have undergone HCT is similar to that for the general population. In most cases, management is primarily supportive, although some patients with severe AKI may require kidney replacement therapy. Early consultation with a nephrologist is advised. (See "Overview of the management of acute kidney injury (AKI) in adults" and "Prevention and management of acute kidney injury (acute renal failure) in children".)

Disease-specific management issues in patients who have undergone HCT include the following:

●Calcineurin inhibitor toxicity – In patients with suspected CNI nephrotoxicity (eg, AKI in the setting of blood CNI levels that are higher than expected), dose reduction or temporary discontinuation of the CNI with close monitoring of trough levels is advised. If discontinued, the CNI may be restarted once AKI resolves. Some HCT specialists choose to switch to another immunosuppressive agent for GVHD prophylaxis (such as sirolimus) if CNI toxicity persists.

●Hepatic sinusoidal obstruction syndrome – The management of AKI in patients with hepatic SOS is mostly supportive and focuses on management of volume overload and maintenance of kidney perfusion. Patients with severe SOS are frequently treated with defibrotide.

A more detailed discussion on the management of hepatic SOS is presented elsewhere. (See "Hepatic sinusoidal obstruction syndrome (veno-occlusive disease) in adults", section on 'Treatment'.)

●Thrombotic microangiopathy – The management of thrombotic microangiopathy after HCT is presented elsewhere in this topic. (See 'Treatment of TA-TMA' below.)

●Viral nephritis – In patients with viral nephritis due to adenovirus or BKPyV, management focuses on treatment of the viral infection. In addition, close monitoring for signs of urinary obstruction induced by hemorrhagic cystitis and/or ureteral stenosis is important to prevent further kidney injury. Viral clearance of adenovirus may be attainable with agents such as cidofovir or brincidofovir. There are presently no effective treatments for BKPyV. BKPyV-specific T cell therapies have been shown to improve hemorrhagic cystitis in one phase II trial; however additional studies are required [22]. Detailed discussions on the treatment of adenovirus and BKPyV infection are presented elsewhere. (See "Diagnosis, treatment, and prevention of adenovirus infection", section on 'Treatment' and "Kidney transplantation in adults: BK polyomavirus-associated nephropathy", section on 'Treatment'.)

Prognosis of AKI — The development of acute kidney injury (AKI) after HCT is associated with a poor short- and long-term prognosis, mainly among patients who require kidney replacement therapy. Mortality rates in patients with severe AKI or who require dialysis vary by treatment modality; in one report, mortality at 6 to 12 months ranged from 7 to 34 to 58 percent for autologous, nonmyeloablative allogeneic, and myeloablative allogeneic HCT, respectively [23]. Another study of 616 patients who underwent allogeneic HCT found a 76 percent mortality among those who required dialysis during hospitalization [2].

AKI requiring dialysis in the peritransplant period has a poor prognosis due, in part, to its association with coexistent injury of multiple other organs [3,4,24-29].

CHRONIC KIDNEY DISEASE — Chronic kidney disease (CKD) is another common kidney complication after hematopoietic cell transplantation (HCT). The reported incidence of CKD following HCT varies widely (0 to over 60 percent at ≥6 months following HCT); this is related in part to variations in the definition of CKD, duration of follow-up, and type of HCT [2,30-32]. In one study of 216 pediatric HCT survivors, CKD (defined as Kidney Disease: Improving Global Outcomes [KDIGO] stage G2 or A2 or more) developed in approximately 17 percent of patients at 10 years post-HCT [33].

Several risk factors have been associated with the development of CKD in this patient population, including acute kidney injury (AKI), total body irradiation exposure and dose, chronic graft-versus-host disease (GVHD), older age, lower glomerular filtration rate (GFR) prior to HCT, female sex, calcineurin inhibitor (CNI) exposure, thrombotic microangiopathy, glomerular disease, hypertension after HCT, and viral infections (such as adenovirus and BK polyomavirus [BKPyV]). Patients with CKD after HCT have lower overall survival rates compared with those without CKD [11,34-36].

The most common causes of CKD in patients who have undergone HCT include chronic CNI toxicity, transplant-associated thrombotic microangiopathy (TA-TMA), and nephrotic syndrome.

Calcineurin inhibitor toxicity — Chronic CNI therapy with tacrolimus or cyclosporine can cause nephrotoxicity similar to that seen in other settings, such as solid organ transplantation. Long-term complications are unusual because CNIs are given in full doses to stable patients for only several months. However, the characteristic vascular and interstitial changes of CNI nephrotoxicity can occur with prolonged therapy for GVHD [37]. Patients undergoing CNI-sparing T cell-depleted (TCD) allogeneic HCT have been shown to have lower rates of kidney failure (defined as median eGFR <60 mL/min/1.73 m2 for ≥100 days any time after 180 days post-HCT) at two years compared with those undergoing conventional allogeneic HCT (31 versus 42 percent) [38].

In patients who develop CKD from chronic CNI therapy, the CNI can generally be continued if kidney function remains relatively stable and ongoing GVHD prophylaxis is needed. However, reducing long-term CNI exposure, if possible, is preferred in order to prevent further progression of CKD. (See "Cyclosporine and tacrolimus nephrotoxicity".)

Thrombotic microangiopathy — TA-TMA (previously known as bone marrow transplant nephropathy) is a potentially life-threatening complication of HCT caused by endothelial injury.

Incidence — The reported incidence of TA-TMA varies widely. While earlier studies reported an incidence of 0.5 to 64 percent [39], more contemporary studies have reported an incidence ranging from 2 to 39 percent [35,40-43]. This wide variation may be explained by the use of different definitions for TA-TMA and the inclusion of both pediatric and adult populations.

Pathogenesis and risk factors — The pathogenesis of TA-TMA is related to endothelial injury, which may be incited by a combination of factors that damage endothelium, including CNIs, chemotherapy, GVHD, total body irradiation, and/or infections, possibly in the setting of abnormalities of the alternative complement pathway [44-46]. Some studies have suggested that TA-TMA may be an "endothelial" manifestation of GVHD [47,48].

Several risk factors for the development of TA-TMA have been described, including older age, female sex, advanced primary cancer disease, unrelated donor transplants, high-dose busulfan conditioning regimen, human leukocyte antigen (HLA) mismatch, nonmyeloablative transplants, total body irradiation, CNI use, mammalian (mechanistic) target of rapamycin (mTOR) inhibitor use in conjunction with CNI use, acute GVHD, and infection [40,49-55].

Clinical presentation — TA-TMA usually develops within the first 100 days after transplantation but may have a later onset in some patients [41,56,57]. Patients typically present with microangiopathic hemolytic anemia along with thrombocytopenia, an elevated serum lactate dehydrogenase (LDH) level, and the presence of schistocytes on the peripheral blood smear. Serum haptoglobin is often low but may be normal or elevated in some patients [41]. Kidney manifestations include an acute or subacute rise in the serum creatinine concentration and a urinalysis that may be relatively normal or show variable proteinuria and/or hematuria. Hypertension is often present. TA-TMA can also be kidney limited with no systemic findings [58-60].

TA-TMA can range from a mild, self-limited form to severe, uncontrolled disease that frequently results in death. The reasons for this variation in disease severity are unclear but may be related to factors involving the recipient, the donor, or inciting events such as infections. In most patients, the hematologic abnormalities eventually resolve, although hypertension and CKD usually persist [7-9,56,61]. Some patients progress to end-stage kidney disease (ESKD) [61,62]. Other patients may develop multiorgan involvement including pulmonary hypertension, polyserositis, gastrointestinal symptoms, and central nervous system injury [63-65].

Evaluation of TA-TMA

Routine surveillance — Many transplant centers routinely screen HCT recipients for transplant-associated thrombotic microangiopathy (TA-TMA), although practice is often center specific. Some centers monitor blood pressure, hemoglobin level, platelet count, serum LDH level, and a urinalysis once or twice weekly during the first few months after HCT.

When to suspect TA-TMA — The diagnosis of transplant-associated thrombotic microangiopathy (TA-TMA) should be suspected in HCT recipients who present with one or more of the following:

●Elevated serum LDH level

●Elevated serum creatinine (or reduction in estimated GFR [eGFR])

●New-onset or increasing proteinuria

●Hypertension that is out of proportion to what would be expected from CNI and glucocorticoid therapy or volume overload (eg, requiring ≥3 antihypertensive medications)

●Sudden requirement for more transfusion support than previously needed to maintain stable blood cell and platelet counts

Initial laboratory testing — In patients who are suspected of having TA-TMA, we obtain the following laboratory tests, if they are not already available:

●Complete blood count and platelet count

●Review of the peripheral blood smear

●Measurement of blood tacrolimus (or cyclosporine) concentration (in patients receiving these agents)

●Serum markers of hemolysis, including LDH and haptoglobin

●Serum complement testing (C3, C4, CH50) and soluble C5b-9 level

●ADAMTS13 activity and inhibitor testing, to exclude the possibility of acquired thrombotic thrombocytopenic purpura (TTP) (see "Diagnosis of immune TTP", section on 'ADAMTS13 testing')

●Urinalysis with examination of the urinary sediment

●Spot urine protein-to-creatinine ratio (or urine microalbumin-to-creatinine ratio)

●Measurement of blood adenovirus, BKPyV, and cytomegalovirus viral loads

Diagnosis of TA-TMA — The diagnosis of transplant-associated thrombotic microangiopathy (TA-TMA) is usually established based upon the presence of characteristic clinical and laboratory findings. Although different diagnostic criteria have been proposed [66-69], there are no uniformly accepted definitions of TA-TMA. Most definitions include a combination of the following:

●Elevated serum LDH level

●Presence of schistocytes on a peripheral blood smear

●Decrease in hemoglobin concentration

●Thrombocytopenia (platelet count <50,000/microL or ≥50 percent reduction from previous counts)

●Decrease in serum haptoglobin

●Negative Coombs test

In cases in which the diagnosis is uncertain based upon clinical findings, a kidney biopsy may be helpful to establish the diagnosis of TA-TMA. The ability to perform a kidney biopsy is often limited by the presence of thrombocytopenia, which increases the risk of bleeding from the biopsy (see "The kidney biopsy", section on 'Thrombocytopenia'). Histologic examination of the kidney reveals mesangiolysis with necrotizing arteriolar and glomerular lesions and intraglomerular and renal arteriolar thrombi.

Treatment of TA-TMA — The optimal approach to the treatment of transplant-associated thrombotic microangiopathy (TA-TMA) is not known. Management is largely supportive and focuses on the management of hypertension and transfusion support as appropriate. Patients with mild disease can be treated in the outpatient setting, although patients with more severe disease often require hospitalization. Kidney replacement therapy with dialysis may be needed in severe cases.

General supportive measures — The following general supportive measures are appropriate, depending upon the patient's clinical status:

●Management of hypertension – Patients with hypertension associated with TA-TMA should receive antihypertensive agents to control blood pressure. The optimal antihypertensive agent for patients with TA-TMA is unclear. In patients with proteinuria, we prefer the use of angiotensin-converting enzyme (ACE) inhibitors or angiotensin receptor blockers (ARB) based upon studies showing a benefit with these agents in patients with nondiabetic CKD. (See "Antihypertensive therapy and progression of nondiabetic chronic kidney disease in adults".)

●Withdrawal of offending agents – Recipients of an allogeneic HCT generally receive a CNI (tacrolimus or cyclosporine) and/or sirolimus for GVHD prophylaxis. These agents have been implicated as risk factors for TA-TMA. We do not routinely discontinue the CNI and/or sirolimus, since there is no evidence that discontinuing these agents is clearly beneficial to patients with TA-TMA. Furthermore, discontinuation of CNIs may increase the risk of GVHD. However, in patients who present with acute kidney injury (AKI), some clinicians would withdraw or reduce the dose of CNI and/or sirolimus if no underlying cause for TA-TMA (eg, GVHD, infection) can be identified and the blood CNI level is higher than expected. If the decision is made to withdraw the CNI and/or sirolimus, replacement with mycophenolate mofetil with or without glucocorticoids may be reasonable. Other replacement options include interleukin (IL) 2 receptor antagonists (such as basiliximab). (See "Prevention of graft-versus-host disease", section on 'Introduction'.)

●Dialysis – Dialysis is performed for standard indications including fluid overload unresponsive to diuretics, hyperkalemia refractory to medical therapy, or metabolic acidosis and uremia. (See "Overview of the management of acute kidney injury (AKI) in adults" and "Kidney replacement therapy (dialysis) in acute kidney injury in adults: Indications, timing, and dialysis dose" and "Prevention and management of acute kidney injury (acute renal failure) in children".)

Additional therapies for severe disease — In patients with severe TA-TMA with kidney, cardiac, or pulmonary involvement that progresses in spite of general supportive measures, potential therapeutic options include rituximab, eculizumab, and defibrotide. Evidence to support their efficacy is limited to mostly small observational studies, and use of these agents should be considered on a case-by-case basis. In patients with severe, progressive TA-TMA with multiorgan involvement who have evidence of complement activation (eg, low serum C3, C4, or CH50 level or elevated soluble C5b-9), we would give eculizumab. In patients with primarily kidney involvement and no evidence of complement activation, we would give rituximab. We reserve the use of defibrotide to patients who do not respond to either eculizumab or rituximab.

●Rituximab – Rituximab, a monoclonal antibody directed against CD20, is frequently used for the treatment of acquired TTP (see "Immune TTP: Initial treatment", section on 'Rituximab'). A number of small case series have shown that treatment with rituximab may induce remission in patients with TA-TMA [70-72]. If rituximab is used, we typically administer 375 mg/m2 weekly for four doses.

●Eculizumab – Eculizumab, a monoclonal antibody directed against the C5 complement component, has been shown to be beneficial in patients with complement-mediated thrombotic microangiopathy. Limited data from observational studies suggest that it may benefit select patients with TA-TMA [73-76]. Dosing and administration of eculizumab for patients with TA-TMA is similar to that for patients with complement-mediated thrombotic microangiopathy. (See "Thrombotic microangiopathies (TMAs) with acute kidney injury (AKI) in adults: CM-TMA and ST-HUS", section on 'Terminal complement blockade'.)

The best data come from an observational study of 64 pediatric HCT recipients with high-risk TA-TMA and multiorgan injury who were treated with eculizumab (median of 11 doses) [73]. TA-TMA resolved at a median of 66 days, and treatment could be safely discontinued. One-year post-HCT survival in this cohort was 66 percent, compared with 17 percent in a previously reported untreated cohort with the same clinical features. Similar benefits have been reported in adult patients with TA-TMA treated with eculizumab [75,76].

●Defibrotide – Defibrotide is a single-stranded oligodeoxyribonucleotide approved for the treatment of severe hepatic sinusoidal obstruction syndrome (see "Hepatic sinusoidal obstruction syndrome (veno-occlusive disease) in adults", section on 'Severe SOS'). In one study of 12 patients with TA-TMA, early use of defibrotide resulted in a complete response in approximately one-half of patients [77].

Unclear role for plasma exchange — There are no convincing data to support the use of plasma exchange in patients who develop TA-TMA, in contrast to the beneficial response seen in patients with acquired TTP [39,57]. Plasma exchange has been tried in selected patients with generally disappointing results [28,39,70,71,78-83].

Monitoring — Patients with TA-TMA should be closely monitored during treatment. We usually follow the hemoglobin level, platelet count, serum LDH level, and serum creatinine to assess the efficacy of therapy and monitor the resolution of TMA. However, there are no markers that have been clearly proven to indicate a successful response to treatment. An increase in the platelet count and/or hemoglobin level, decrease in the LDH level, reduced need for blood or platelet transfusions, and recovery of kidney function can be interpreted as signs of improvement.

Prognosis — TA-TMA frequently has a poor prognosis with a mortality rate as high as 50 to 60 percent [39,50,68,84,85]. The exact reason for this high mortality is unclear but may be related to direct complications of endothelial injury involving multiple organs (kidney, lung, or heart) and/or complications of acute GVHD and infection. Improvement of thrombotic microangiopathy has been associated with a lower risk of death [85].

Factors predictive of a poor prognosis in TA-TMA include age >18 years, the use of an unrelated or haploidentical donor, schistocyte count (>5 to 10 per high-powered-field), and kidney involvement [49,53,57,84].

Nephrotic syndrome — There are several case reports and case series of nephrotic syndrome following HCT [30,86-95]. As an example, in one series of 163 patients who underwent HCT, nephrotic syndrome developed in seven (4.3 percent) a median of 300 days after HCT [87].

Pathology and pathogenesis — A variety of histologic patterns have been reported; the most common is membranous nephropathy (MN), followed by minimal change disease (MCD) [87,88,96,97]. This was illustrated in a systematic review of 116 cases: 66 percent had MN, and 19 percent had MCD [97]. Less common kidney biopsy findings include focal segmental glomerulosclerosis, immunoglobulin A (IgA) nephropathy, and mesangial proliferative disease.

Most patients with HCT-associated MN are negative for anti-phospholipase A2 receptor (PLA2R) antibodies [98] although rare cases of PLA2R-positive MN after HCT have been reported [99,100]. Among those with PLA2R-negative MN, one study has found that between 83 and 100 percent have antibodies directed against the glomerular target antigen protocadherin FAT1 (FAT1) [101], suggesting that FAT1-associated MN may represent a unique subset of HCT-associated MN. Case reports of neural epidermal growth factor-like 1 (NELL1)-associated MN [102] as well as MN with extensive tubular basement membrane (TBM) deposits accompanied by acute tubular injury and tubulointerstitial inflammation have also been described among HCT recipients [103]. In the latter, antibodies generated against yet-to-be-discovered shared or different glomerular and TBM components are thought to explain the pathogenesis of these cases.

The occurrence of PLA2R-negative MN is often associated with a decrease in immunosuppression and an increased likelihood of GVHD (alloimmune MN). A proposed mechanism is immune dysregulation from transfer of alloreactive donor lymphocytes with reactivity toward glomerular antigens [104]. In one literature review, nephrotic syndrome was diagnosed 8 to 14 months following HCT, and all 42 cases occurred within two months following the diagnosis of GVHD [88]. However, other studies have questioned the association between GVHD and nephrotic syndrome after HCT [95].

Evaluation and diagnosis — We generally perform a kidney biopsy in all patients who develop nephrotic syndrome after HCT to establish the diagnosis and pattern of glomerular injury. The ability to perform a kidney biopsy may be limited by the presence of thrombocytopenia, which is common in patients who have undergone HCT and increases the risk of bleeding from the biopsy. However, with careful planning and platelet transfusion, a kidney biopsy can be performed safely. (See "The kidney biopsy", section on 'Thrombocytopenia'.)

Additional evaluation is guided by the findings on kidney biopsy:

●In patients with MN, we obtain a serum anti-PLAR2 antibody level (by enzyme-linked immunosorbent assay [ELISA]). A positive anti-PLA2R antibody test supports the diagnosis of primary PLA2R-associated MN. (See "Membranous nephropathy: Clinical manifestations and diagnosis", section on 'Diagnostic utility' and "Membranous nephropathy: Pathogenesis and etiology", section on 'Phospholipase A2 receptor'.)

●In patients with MCD, we evaluate for other secondary causes of MCD, such as drugs, neoplasms, and infections. In particular, the patient should be assessed for the possibility of recurrent hematologic malignancy after HCT, which may be an inciting factor for the development of MCD. (See "Minimal change disease: Etiology, clinical features, and diagnosis in adults", section on 'Etiology'.)

Treatment and monitoring — There is no high-quality evidence to guide the optimal therapy of patients with nephrotic syndrome after HCT. In patients with a known history of GVHD, remission of nephrotic syndrome may occur upon reinitiation of immunosuppressive therapy used for chronic GVHD, which may include a CNI, mycophenolate mofetil, or even cyclophosphamide. However, treatment with additional immunosuppressive agents is frequently needed to induce remission. Our treatment approach, which is based primarily upon low-quality evidence and our clinical experience, is described below.

Membranous nephropathy — Patients with biopsy-proven MN who are anti-PLA2R antibody positive should be treated with the same approach as that used for patients with primary PLA2R-associated MN. (See "Membranous nephropathy: Treatment and prognosis", section on 'Initial therapy for primary MN'.)

In patients with biopsy-proven MN who are anti-PLA2R antibody negative, we suggest rituximab as initial immunosuppressive therapy. If rituximab is not available, a CNI (tacrolimus or cyclosporine, if not already given for GVHD) is an alternative option. We do not give glucocorticoid monotherapy given the variable response in patients with HCT-associated MN [105,106] and its lack of effectiveness among patients with primary MN. Dosing of rituximab for HCT-associated MN is similar to that used for patients with primary MN. All other immunosuppressive therapies that are used to prevent chronic GVHD are continued among patients who receive rituximab. (See "Membranous nephropathy: Treatment and prognosis", section on 'Rituximab'.)

There is no high-quality evidence to support our approach. Our preference for rituximab is based upon observational studies supporting its use in patients with HCT-associated MN or refractory chronic GVHD [103,105,107-112] as well as indirect evidence from randomized trials showing a benefit in patients with primary MN. (See "Membranous nephropathy: Treatment and prognosis", section on 'Moderate risk of progression'.)

We measure serum creatinine, serum albumin, and 24-hour urine protein excretion monthly to monitor the response to therapy. The response to rituximab generally occurs within a few months but may take up to 6 to 12 months. An increase in serum albumin and consistent decrease in proteinuria are regarded as a positive response. If no improvement in either of these parameters is seen by six months, we administer a second course of rituximab. In patients who do not respond to two courses of rituximab, we switch to a CNI.

Minimal change disease — Patients with biopsy-proven MCD who are found to have a secondary cause should be treated as appropriate for the underlying cause. As an example, if the patient is found to have recurrence of their hematologic malignancy, therapy should be directed at treating the underlying malignancy.

In patients with biopsy-proven MCD who do not have another identifiable secondary cause (other than HCT), we suggest oral glucocorticoid therapy as initial immunosuppressive therapy. Our approach is similar to the initial therapy for patients with primary MCD, which is discussed in detail elsewhere (see "Minimal change disease: Treatment in adults", section on 'Glucocorticoid monotherapy'). If the patient does not respond to or wishes to avoid glucocorticoid therapy, rituximab or a CNI (tacrolimus or cyclosporine, if not already given for GVHD) is a reasonable alternative.

There is no high-quality evidence to support our approach, which is based primarily upon indirect evidence from trials showing a benefit to glucocorticoids in patients with primary MCD. (See "Minimal change disease: Treatment in adults", section on 'Glucocorticoid monotherapy'.)

We measure serum creatinine, serum albumin, and 24-hour urine protein excretion monthly to monitor the response to therapy. The response to glucocorticoids generally occurs within a few weeks to months. An increase in serum albumin and consistent decrease in proteinuria are regarded as a positive response. If no improvement in either of these parameters is seen by three months, we switch to rituximab or a CNI.

KIDNEY TRANSPLANTATION — Hematopoietic cell transplantation (HCT) recipients who develop end-stage kidney disease (ESKD) and have maintained remission from their hematologic malignancy may be suitable candidates for kidney transplantation. However, data on outcomes after kidney transplantation in this patient population are limited [113-115]. In one multicenter study of 67,578 allogeneic HCT recipients, 45 underwent solid organ transplantation (15 kidney) after HCT [114]. The median time from HCT to kidney transplantation was 84 months, with a majority receiving living-related donor kidneys; three received a kidney transplant from the HCT donor and were off immunosuppressive therapy at last follow-up. Five-year overall survival was 100 percent; 4 of 15 patients developed kidney allograft rejection. Similar survival rates have been reported among pediatric HCT recipients who underwent kidney transplantation [113].

One major concern about kidney transplantation after HCT is the associated immunosuppression needed to avoid rejection, given the possible increased risk of cancer relapse or secondary malignancies. However, in the multicenter study cited above, only 2 of 28 patients with malignant disease who received a kidney transplant after HCT had a relapse of their cancer [114].

Combined HCT and kidney transplantation has been shown to result in the development of tolerance to the transplanted kidney and withdrawal of immunosuppressive medications [116,117].

The general approach to the evaluation of the potential kidney transplant recipient is presented separately. (See "Kidney transplantation in adults: Evaluation of the potential kidney transplant recipient".)

SOCIETY GUIDELINE LINKS — Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Acute kidney injury in adults" and "Society guideline links: Thrombotic microangiopathies (TTP, HUS, and related disorders)".)

SUMMARY AND RECOMMENDATIONS

●Acute kidney injury – Acute kidney injury (AKI) occurs in approximately 50 percent of patients following hematopoietic cell transplantation (HCT). In general, allogeneic HCT is associated with a higher risk of AKI than autologous HCT, and myeloablative conditioning regimens are associated with a higher risk compared with nonmyeloablative regimens. (See 'Incidence and risk factors' above.)

•Causes – The most common causes of AKI after HCT are prerenal disease, acute tubular necrosis, toxicity from medications (such as calcineurin inhibitors [CNIs]), hepatic sinusoidal obstruction syndrome (SOS), thrombotic microangiopathy, and viral infections (such as BK polyomavirus [BKPyV], adenovirus, and cytomegalovirus). Less frequent causes of AKI include tumor lysis syndrome and acute engraftment syndrome. In addition, AKI after HCT may result from more than one of these etiologies. (See 'Causes of AKI' above.)

•Evaluation – The evaluation of AKI among patients who have undergone HCT is similar to that for the general population and includes a thorough history and physical examination, examination of the urinalysis and sediment and urine chemistry, and imaging of the kidneys (algorithm 1). In addition, the evaluation should include an assessment for transplant-specific causes of AKI. (See 'Evaluation of AKI' above.)

•Management – In general, the overall management of AKI among patients who have undergone HCT is similar to that for the general population. In most cases, management is primarily supportive, although some patients with severe AKI may require kidney replacement therapy. Early consultation with a nephrologist is advised. (See 'Management of AKI' above.)

●Chronic kidney disease – Chronic kidney disease (CKD) may occur following HCT and is most commonly due to chronic CNI nephrotoxicity, transplant-associated thrombotic microangiopathy (TA-TMA), and nephrotic syndrome. (See 'Chronic kidney disease' above.)

•Calcineurin inhibitor nephrotoxicity – Chronic CNI therapy with tacrolimus or cyclosporine can cause nephrotoxicity similar to that seen in other settings, such as solid organ transplantation. Long-term complications are unusual because CNIs are given in full doses to stable patients for only several months. (See 'Calcineurin inhibitor toxicity' above.)

•Transplant-associated thrombotic microangiopathy – TA-TMA is a potentially life-threatening complication of HCT caused by endothelial injury. TA-TMA usually develops within the first 100 days after transplantation but may have a later onset in some patients.

-Clinical presentation – Patients typically present with microangiopathic hemolytic anemia along with thrombocytopenia, an elevated serum lactate dehydrogenase (LDH) level, and the presence of schistocytes on the peripheral blood smear. Serum haptoglobin is often low but may be normal or elevated in some patients. Kidney manifestations include an acute or subacute rise in the serum creatinine concentration and a urinalysis that may be relatively normal or show variable proteinuria and/or hematuria. Hypertension is often present. TA-TMA can range from a mild, self-limited form to severe, uncontrolled disease that frequently results in death. (See 'Clinical presentation' above.)

-Diagnosis – The diagnosis of TA-TMA should be suspected in HCT recipients who present with one or more of the following: elevated LDH level, elevated serum creatinine, new-onset or increasing proteinuria, hypertension that is out of proportion to what would be expected from CNI and glucocorticoid therapy or volume overload (eg, requiring ≥3 antihypertensive medications), or sudden requirement for more transfusion support than previously needed to maintain stable blood cell and platelet counts. The diagnosis of TA-TMA is usually established based upon the presence of characteristic clinical and laboratory findings. In cases in which the diagnosis is uncertain based upon clinical findings, a kidney biopsy may be helpful. (See 'Evaluation of TA-TMA' above.)

-Management – The optimal approach to the treatment of TA-TMA is not known. Management is largely supportive and focuses on the management of hypertension and transfusion support as appropriate. Patients with mild disease can be treated in the outpatient setting, although patients with more severe disease often require hospitalization. In patients with TA-TMA who are taking a CNI and/or sirolimus, we suggest not discontinuing these agents (Grade 2C). Plasma exchange has not been shown to be effective. Potential therapeutic options for patients with severe TA-TMA include rituximab, eculizumab, and defibrotide, although evidence to support their efficacy is limited. Kidney replacement therapy with dialysis may also be needed in severe cases. (See 'Treatment of TA-TMA' above.)

•Nephrotic syndrome – Nephrotic syndrome, most commonly associated with membranous nephropathy (MN) or minimal change disease (MCD), can occur following HCT and appears to be related to graft-versus-host disease (GVHD). The optimal therapy of patients with nephrotic syndrome after HCT is unknown. In patients with a known history of GVHD, remission of nephrotic syndrome may occur upon reinitiation of immunosuppressive therapy, but additional immunosuppressive agents are frequently needed to induce remission. In patients with biopsy-proven MN who are anti-phospholipase A2 receptor (PLA2R) negative, we suggest rituximab as initial immunosuppressive therapy (Grade 2C). In patients with biopsy-proven MCD without an identifiable secondary cause (other than HCT), we suggest oral glucocorticoids as initial immunosuppressive therapy (Grade 2C). (See 'Nephrotic syndrome' above.)

ACKNOWLEDGMENT — The UpToDate editorial staff acknowledges Chirag Parikh, MD, PhD, who contributed to an earlier version of this topic review.

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  108. Byrne-Dugan CJ, Collins AB, Lam AQ, Batal I. Membranous nephropathy as a manifestation of graft-versus-host disease: association with HLA antigen typing, phospholipase A2 receptor, and C4d. Am J Kidney Dis 2014; 64:987.
  109. Troxell ML, Pilapil M, Miklos DB, et al. Renal pathology in hematopoietic cell transplantation recipients. Mod Pathol 2008; 21:396.
  110. Vischini G, Cudillo L, Ferrannini M, et al. Rituximab in post allogeneic hematopoietic stem cell transplantation membranous nephropathy: a case report. J Nephrol 2009; 22:160.
  111. Mattei D, Sorasio R, Guarnieri A, et al. Long-term results of rituximab treatment for membranous nephropathy after allogeneic hematopoietic SCT: a case report. Bone Marrow Transplant 2010; 45:1111.
  112. Ferrannini M, Vischini G, Di Daniele N. Rituximab in membranous nephropathy after haematopoietic stem cell transplantation. Nephrol Dial Transplant 2008; 23:2700.
  113. Faraci M, Bertaina A, Dalissier A, et al. Solid organ transplantation after hematopoietic stem cell transplantation in childhood: A multicentric retrospective survey. Am J Transplant 2019; 19:1798.
  114. Koenecke C, Hertenstein B, Schetelig J, et al. Solid organ transplantation after allogeneic hematopoietic stem cell transplantation: a retrospective, multicenter study of the EBMT. Am J Transplant 2010; 10:1897.
  115. Butcher JA, Hariharan S, Adams MB, et al. Renal transplantation for end-stage renal disease following bone marrow transplantation: a report of six cases, with and without immunosuppression. Clin Transplant 1999; 13:330.
  116. Scandling JD, Busque S, Dejbakhsh-Jones S, et al. Tolerance and chimerism after renal and hematopoietic-cell transplantation. N Engl J Med 2008; 358:362.
  117. Issa F, Strober S, Leventhal JR, et al. The Fourth International Workshop on Clinical Transplant Tolerance. Am J Transplant 2021; 21:21.
Topic 7197 Version 35.0

References

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60 : Kidney Biopsy Findings Among Allogenic Hematopoietic Stem Cell Transplant Recipients With Kidney Injury: A Case Series.

61 : Clinical course of late-onset bone marrow transplant nephropathy.

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65 : Clinicopathological manifestations and treatment of intestinal transplant-associated microangiopathy.

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99 : Detection of anti-PLA2R autoantibodies and IgG subclasses in post-allogeneic hematopoietic stem cell transplantation membranous nephropathy.

100 : The Case | Proteinuria in a patient with hematopoietic stem cell transplantation.

101 : Hematopoietic Stem Cell Transplant-Membranous Nephropathy Is Associated with Protocadherin FAT1.

102 : NELL1-Associated Membranous Glomerulopathy After Hematopoietic Stem Cell Transplantation.

103 : Membranous Nephropathy With Extensive Tubular Basement Membrane Deposits Following Allogeneic Hematopoietic Cell Transplant: A Report of 5 Cases.

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106 : The Management of Membranous Glomerulopathy in Allogeneic Stem Cells Transplantation: Updated Literature

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108 : Membranous nephropathy as a manifestation of graft-versus-host disease: association with HLA antigen typing, phospholipase A2 receptor, and C4d.

109 : Renal pathology in hematopoietic cell transplantation recipients.

110 : Rituximab in post allogeneic hematopoietic stem cell transplantation membranous nephropathy: a case report.

111 : Long-term results of rituximab treatment for membranous nephropathy after allogeneic hematopoietic SCT: a case report.

112 : Rituximab in membranous nephropathy after haematopoietic stem cell transplantation.

113 : Solid organ transplantation after hematopoietic stem cell transplantation in childhood: A multicentric retrospective survey.

114 : Solid organ transplantation after allogeneic hematopoietic stem cell transplantation: a retrospective, multicenter study of the EBMT.

115 : Renal transplantation for end-stage renal disease following bone marrow transplantation: a report of six cases, with and without immunosuppression.

116 : Tolerance and chimerism after renal and hematopoietic-cell transplantation.

117 : The Fourth International Workshop on Clinical Transplant Tolerance.

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