AUTHOR AND EDITOR INFORMATION

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• Follow-up
• Miscellaneous
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INTRODUCTION

Section 2 of 11  

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Background

Radiation nephritis is kidney injury and impairment of function caused by ionizing radiation. It may occur after irradiation of one or both kidneys, and it may result in kidney failure.

Classic radiation nephritis occurs after bilateral local kidney irradiation. It is a syndrome of chronic renal failure occurring months or years after renal irradiation (Luxton, 1961). Acute radiation nephritis develops 6-12 months after irradiation, whereas chronic radiation nephritis develops years later. Radiation nephritis has recently been discovered to cause chronic renal failure after bone marrow transplantation (BMT) (Cohen, 2000). In addition, the use of yttrium–90–tagged (⁹⁰Y-tagged) somatostatin and other radionuclides for radionuclide therapy cause radiation nephritis when they are filtered by the kidneys and reabsorbed by the renal tubule epithelium or when blood-borne exposure to the kidney cells occurs (Cohen, 2001).

The term nephritis was commonly used in the past; however, because radiation nephropathy is not an inflammatory condition, the term nephropathy is probably more appropriate. For older reports, the term nephritis will be used.

Pathophysiology

Radiation nephritis is due to cellular injury caused by ionizing radiation. All components of the kidney are affected, including the glomeruli, blood vessels, tubular epithelium, and interstitium (Cohen and Robbins, 2003).

In the case of local kidney irradiation or total-body irradiation, the injury is direct. In the case of injury by radionuclide therapy, a radioactive substance can injure the kidneys if its pharmacokinetics cause it to lodge in the kidney during a time when it is still a radioemitter. This is the case for the ⁹⁰Y-tagged somatostatin, which has been used for treatment of neuroendocrine malignancies, and also for holmium-166–tagged (¹⁶⁶Ho-tagged) phosphonate 1,4,7,10-tetraazacyclododecane-1,4,7,10-tetramethylene phosphonic acid (DOTMP) (Moll, 2001; Giralt, 2003).

Oxidative injury to the DNA initiates injury to healthy tissue by ionizing radiation. This is a genotoxic injury. A cell with sufficient DNA injury eventually dies after several divisions. The delay in cell death may partially explain why radiation injury to healthy tissue is a delayed reaction.

The detailed mechanism whereby the kidney cells and tissues malfunction after this injury remains poorly understood. In experimental models, ultrastructural damage to the glomerular endothelium is observed 3 weeks after a 10-Gy (1000-rad) dose of local kidney irradiation and neutrophil adherence to the endothelium occurs (Cohen and Robbins, 2003). By 6-10 weeks after the same dose, a wave of tubular epithelial cell death occurs. This is followed by interstitial scarring. The scarring tends to be most severe in the outer cortex, and it proceeds inward. The progression of these events is accelerated with higher doses of radiation.

The earliest functional evidence of experimental radiation nephropathy is proteinuria, which is evident by 6 weeks in a radiation nephritis model with 17-Gy total-body irradiation. Azotemia and hypertension both are present by 12-15 weeks in the same model. The origin of the hypertension probably is similar to that of most experimental hypertension, though pressure-natriuresis curves have not been studied. Renin levels in systemic blood are normal or low, and blood and intrarenal angiotensin II levels are within the reference range (ie, not elevated).

On clinical observation, radiation nephritis does not occur until months after the kidneys are exposed to sufficient ionizing radiation. Early data suggested that a dose of 20 Gy (2000 rads) given in multiple fractions over several weeks causes radiation nephritis (Luxton, 1961).

Radiation nephritis after BMT (BMT nephropathy) occurs after a lower dose of irradiation than what was traditionally accepted. This dose is given over days, not weeks, to the whole body (total-body irradiation) and is accompanied by chemotherapy, which may account for the unexpectedly dramatic effect on the kidneys. Proteinuria is usual though generally not in the nephrotic range. Azotemia and hypertension also develop. Anemia out of proportion to the degree of azotemia is a characteristic finding. Severe cases may be associated with a hemolytic- or uremic-like picture, with thrombocytopenia, microangiopathic hemolytic anemia, and a high blood level of lactate dehydrogenase (LDH). This last syndrome may be the result of severe endothelial injury.

In the case of unilateral renal irradiation, progressive scarring of the irradiated kidney may occur, with severe hypertension related to renin release by the irradiated kidney.

Frequency

United States

Radiation nephritis does not occur in all irradiated patients. In the large British series of classic radiation nephritis described by Luxton, only 20% of subjects developed radiation nephritis, though each received more than 2500 rads to the kidneys.

The form of radiation nephritis in patients who receive BMT occurs in 10-20% of these patients.

In a report from Seattle, Wash, 30 of 83 subjects treated with ¹⁶⁶Ho to DOTMP developed some kidney injury; 7 subjects had thrombotic microangiopathy (ie, hemolytic uremic syndrome) (Giralt, 2003).

International

No international variability is apparent in radiation nephritis, except as determined by the use of therapeutic irradiation.

Mortality/Morbidity

As with other causes of chronic renal failure, radiation nephritis may be asymptomatic. When it sufficiently reduces kidney function, symptoms and signs of renal failure occur. End-stage renal disease and the need for dialysis or transplantation may develop. In patients with BMT nephropathy who are receiving dialysis, the survival rate is less than that of age-matched control subjects (Cohen, 1998).

• Proteinuria occurs, but it is usually not a striking feature in patients with radiation nephritis. Reports of classic radiation nephritis generally describe non–nephrotic-range proteinuria ( <3 g/d). In BMT nephropathy, the average urinary protein level has been reported at 2.5 g/d.
• Hypertension is a typical feature. In classic radiation nephritis, malignant hypertension may affect as many as 30% of patients and can occur as late as 11 years after irradiation. In BMT nephropathy, hypertension is a cardinal feature and observed along with azotemia. Were it not for antihypertensive agents, malignant hypertension would probably be a major feature of BMT nephropathy.
• On hematologic analysis, accompanying anemia is present in both radiation nephritis and BMT nephropathy and is more severe than that expected for the degree of azotemia. In severe cases of BMT nephropathy, hemolytic anemia, a high blood LDH level, and a decreased platelet count may be present. This syndrome may be mistaken for hemolytic-uremic syndrome (HUS) or thrombotic thrombocytopenic purpura (TTP).

Race

No data on the racial variance of radiation nephritis have been published.

Sex

No confirmed sex-based differences in radiation nephritis have been reported. At the BMT unit of the Medical College of Wisconsin, BMT nephropathy has affected more women than men, but other centers have not had this experience.

Age

No age-based differences in susceptibility to classic radiation nephritis have been confirmed. However, in the case of BMT nephropathy, children appear to be more likely to develop this syndrome than adults.

CLINICAL

Section 3 of 11  

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History

• Previous exposure to a sufficient dose of ionizing radiation is a necessary element in the patient's history. External-beam irradiation is usually a clear-cut feature in the history, and it should have encompassed the kidney areas. Use of a radioactive isotope, in therapeutic doses, may not be obvious.
• Classic radiation nephritis requires exposure of the kidneys to x-rays or gamma rays in a dose higher than 2000 cGy (rads). However, radiation nephritis does not always ensue after the kidneys are irradiated.
• Newer x-ray therapies are sharply focused on the area to be treated; therefore, it is unlikely that the kidneys are irradiated in a case of uterine cervical irradiation, for instance.
• In patients who have undergone BMT, a history of total-body irradiation for pre-BMT conditioning should be determined. Partial renal shielding reduces but does not eliminate the risk of BMT nephropathy.
• Because radiation nephritis is a delayed injury, renal disease that quickly follows kidney irradiation (ie, within hours or days) is usually caused by some other factor.
• • Classic acute radiation nephritis occurs 6-12 months after irradiation, and chronic radiation nephritis may not develop for years.
  • Similarly, proteinuria or hypertension ascribed to radiation nephritis does not develop for months or years.
• Expected symptoms of radiation nephritis and BMT nephropathy are the same as those observed in patients with chronic renal disease.
• • Nocturia may develop due to the loss of urine concentrating ability.
  • Retention of salt and water may lead to edema and an increase in blood pressure.
  • Anemia may occur, with fatigue, dyspnea, and loss of endurance.
  • Loss of appetite, nausea, and weight loss may occur when there is a severe reduction in renal function.
  • Itching may occur with advanced renal failure, that is, stage V chronic kidney disease (see Staging).

Physical

• Hypertension, often severe, is a major feature of radiation nephritis. It may be the only clinical feature.
• Blood-pressure elevation can be significant. When this elevation is associated with end-organ damage, such as eyeground changes or encephalopathy, it is termed malignant. Malignant hypertension has been reported in radiation nephropathy.
• Long-standing hypertension may result in left ventricular enlargement or hypertrophy, which may be detectable on examination. Findings on physical examination are not specific for radiation nephritis or BMT nephropathy.

Causes

• The essential component for causing radiation nephritis is sufficient exposure of the kidneys to ionizing radiation.
• BMT nephropathy is also caused by irradiation, though histologic changes, similar to those of BMT nephropathy, were described in a single patient who had undergone BMT and who had chemotherapy-based pre-BMT conditioning without irradiation.
• Not all patients exposed to sufficient renal irradiation develop renal injury. The reason for this clinical variability is unknown.
• The heterogeneity of response of healthy tissue to ionizing radiation is poorly understood. No reliable clinical predictors are available for the development of radiation nephritis. Some individuals may develop radiation nephritis at a dose of radiation that has no clinical effect on others.

DIFFERENTIALS

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Other Problems to be Considered

Cyclosporine or tacrolimus toxicity
Pamidronate-induced focal glomerulosclerosis

WORKUP

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Lab Studies

• Tests of blood urea nitrogen and serum creatinine levels
• • These tests help in assessing overall kidney function and are correlated with the glomerular filtration rate (GFR).
  • By using patient age and weight, the Cockcroft-Gault formula enables calculation of the creatinine clearance from the plasma creatinine, without a 24-hour urine collection. This should be used only if the patient has a stable plasma creatinine level. This formula does not apply to patients with acute renal failure. The abbreviated Modification of Diet in Renal Disease (MDRD) formula may be used to estimate the glomerular filtration rate (Stevens, 2006); it is not known whether this formula is preferable to the Cockcroft-Gault formula.
• Determination of urine protein level in a 24-hour specimen or spot urine protein specimen
• • The protein-to-creatinine ratio provides an estimate of the amount of protein in the urine over a 24-hour period.
  • The values help in assessing the degree of proteinuria.
  • A 24-hour urine protein value higher than 3 g or more than 2 g per gram of urinary creatinine is in the nephrotic range.
  • Nephrotic-range proteinuria may suggest a diagnosis other than radiation nephritis or BMT nephropathy. For instance, focal glomerulosclerosis can occur in subjects who have undergone BMT and then treatment with pamidronate. In these cases, the urine protein excretion may be high, even as high as 10 g/d (Markowitz, 2001).
• Urinalysis
• • Results may support renal parenchymal injury by showing granular casts.
  • The presence of red cell casts is not consistent with radiation nephritis or BMT nephropathy and instead suggests acute glomerulonephritis.
• Other studies may be useful for the differential diagnosis of renal failure with nephrotic-range proteinuria and should be ordered according to the clinical presentation.
  • Serum complement testing
  • Antinuclear antibody measurement
  • Antineutrophil cytoplasmic antibody measurement
  • Hepatitis panel
  • Protein electrophoreses
• Determination of CBC count
• • This test helps evaluate the degree of anemia and/or thrombocytopenia.
  • In BMT nephropathy, lower platelet counts correlate with a more rapid decline in renal function.
  • In less severe cases, the drop in the platelet count is transient.
• Test of plasma LDH level
• • This level has been correlated with the rapidity of renal failure in BMT nephropathy.
  • The increased LDH level in BMT nephropathy may be transient.
• Test of plasma potassium level
• • Hyperkalemia (>5 mmol/L) may occur in BMT nephropathy, even in subjects not taking angiotensin-converting enzyme (ACE) inhibitors, angiotensin II-receptor blockers (ARBs), or cyclosporine A.
  • Further studies may show that the fractional excretion of potassium may be lower than expected for the degree of azotemia, and the plasma aldosterone level may be low.

Imaging Studies

• Kidney ultrasonography
• • Sonography helps in ruling out urinary tract obstruction.
  • A reduction in kidney size occurs over time. Images show smaller kidneys with capsular thickening consistent with chronic radiation nephropathy.
• Chest radiography
• • Long-standing or severe hypertension may cause cardiac enlargement with left ventricular hypertrophy.
  • With advanced renal failure and fluid retention, pleural effusions and/or interstitial edema may be present.

Other Tests

• Monitoring blood pressure for 24 hours (ambulatory blood-pressure monitoring) may help differentiate true hypertension from white-coat hypertension.

Procedures

• Although not necessary in every case, kidney biopsy allows histologic confirmation of the diagnosis.
• Biopsy can be performed percutaneously or transvenously.
• Biopsy may be associated with bleeding complications in cases of thrombocytopenia (platelet count <100,000/µL) or if blood pressure is excessively high (>160/100 mm Hg).

Histologic Findings

In classic radiation nephritis, arterial and arteriolar thickening is present, and arteriolar fibrinoid necrosis or ischemic and sclerotic glomerular changes are possible. Interstitial fibrosis is also present. Early descriptions of radiation nephritis note glomerular hypocellularity and cellular degeneration. Electron microscopy shows endothelial degeneration and subendothelial expansion by electron-lucent material (Keane, 1976).

In BMT nephropathy, glomerular mesangiolysis, or loss of mesangial cells and rarefaction of the mesangial matrix, develops. Tubular atrophy and interstitial fibrosis may be present. Arteriolar fibrinoid necrosis has been described. As in classic radiation nephritis, electron microscopy shows both subendothelial expansion by electron-lucent material and endothelial degeneration. A similar appearance is described in cases of renal failure that occurred after radioisotope internal radiotherapy.

Proliferative crescentic glomerulonephritis has been reported as a rare, late complication of BMT. Kidney biopsy shows glomerular hypercellularity with crescent formation.

Staging

The stages of radiation nephropathy in terms of kidney function are the same as those of all chronic kidney diseases.

• Stage I - GFR 90 mL/min or better but injury present
• Stage II - GFR 60-89 mL/min
• Stage III - GFR 30-59 mL/min
• Stage IV - GFR 15-29 mL/min
• Stage V - GFR <15 mL/min or dialysis needed

TREATMENT

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Medical Care

As with chronic renal disease of any kind, the major risk is progressive loss of renal function with evolution to end-stage renal failure. Concomitant hypertension predisposes patients to stroke and heart disease. Uncontrolled hypertension may accelerate the loss of renal function. To slow the progression of renal disease, strict control of blood pressure must be maintained; this is also true for radiation nephritis and BMT nephropathy.

• An estimate of the rate of kidney function loss can be made by graphing the reciprocal of the plasma creatinine versus time. The X intercept on the graph is a guide to when the patient will have reached end-stage renal failure, requiring a form of renal replacement therapy, such as dialysis or transplantation (Cohen, 1991).
• • The graph of 100/plasma creatinine yields a number that varies directly with the GFR and that is a fair estimate of the GFR.
  • The graph of 100/plasma creatinine versus time in BMT nephropathy may be biphasic, with a rapid phase followed by a slower phase.
  • Such graphs can be made by using spreadsheet programs, such as Microsoft Excel.
• Antihypertensive agents are an important part of clinical management for radiation nephritis or BMT nephropathy. The goal of therapy is to control the blood pressure to remain less than 130/85 mm Hg or 125/75 mm Hg if the patient has proteinuria of greater than 1000 mg/d.
• • No proof suggests that one type of antihypertensive agent is superior to another in these specific conditions. Nonetheless, ACE inhibitors are favored because of their known benefit in other progressive kidney diseases (Choi, 2005). An angiotensin II blocker was shown to be very effective in a single recent case of radiation nephropathy (Cohen, 2003).
  • In experimental studies of radiation nephritis, ACE inhibitors and ARBs are particularly effective in the treatment and prevention of histological injury and renal function loss (Moulder, 1998). Conversely, angiotensin II infusion in experimental radiation nephritis models has distinct adverse effects.
• Patients with radiation nephritis or BMT nephropathy may be more anemic than expected for their level of renal function. Anemia may be treated with subcutaneous injections of erythropoietin.

Consultations

No specific consultations are necessary other than those that may arise from intercurrent illness. A patient who has undergone BMT may have other medical problems, such as hypothyroidism, cataracts, or bone avascular necrosis. Secondary cancers are a substantial risk, so ongoing oncological follow-up is essential.

Diet

Salt restriction probably helps control hypertension in cases of radiation nephritis or BMT nephropathy. Patients must avoid instant, processed, or snack foods, and they must not use salt in cooking or at the dining table.

Activity

No specific activity restrictions are necessary.

MEDICATION

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Control of hypertension and treatment of anemia are necessary. In BMT nephropathy, the occurrence of hyperkalemia requires additional attention. For control of hypertension, ACE inhibitors are preferred, but they may raise the serum potassium level and should be avoided if the patient is hyperkalemic. Other antihypertensives, such as calcium channel blockers and diuretics, may be used to control blood pressure. Experience at the authors' center is that 75% of patients require diuretics for control of their blood pressure.

Drug Category: ACE inhibitors

These agents reduce the systemic arterial blood pressure, reducing injury caused by elevated blood pressure. They may not only reduce cardiovascular risk but also slow progression of renal failure. ACE inhibitors may also slow progression of renal failure by lowering intraglomerular pressure or other intrarenal mechanisms.

Drug Category: Angiotensin II receptor antagonists

Antagonize the action of angiotensin II at the type 1 receptor, reducing systemic arterial blood pressure and blunting the intrarenal effect of angiotensin II. If ACE inhibitors cause cough, ARBs may be substituted.

Drug Category: Calcium channel blockers

Antihypertensive agents other than or in addition to ACE inhibitors and ARBs may be needed for blood-pressure control in many subjects with hypertension and chronic renal failure. The same is true for subjects with radiation nephritis. No evidence indicates that one type of calcium channel blocker is preferred over another for radiation nephritis. However, one should avoid verapamil because use of this drug in a subject with hyperkalemia may cause atrial arrest.

Drug Category: Cation exchange resins

Hyperkalemia may occur in subjects with BMT nephropathy, whether or not they are simultaneously taking ACE inhibitors or ARBs. For life-threatening hyperkalemia (plasma K > 6 mmol/L and/or ECG changes), emergency measures, such as intravenous glucose and insulin, may be needed. For persistent, lesser degrees of hyperkalemia, a cation exchange resin may be needed to remove potassium by means of the gut.

Drug Category: Mineralocorticoids

Impaired potassium excretion in BMT nephropathy may be associated with low blood levels of aldosterone. In other causes of chronic renal failure with such aberrant potassium metabolism, use of a synthetic mineralocorticoid has been helpful.

Drug Category: Erythropoietins

Anemia may occur in both radiation nephritis and BMT nephropathy, which has been associated with low blood levels of endogenous erythropoietin. Treatment of anemia with exogenous erythropoietin may relieve symptoms of anemia.

Drug Category: Diuretics

Control of hypertension in radiation nephritis and most chronic renal disease requires use of a diuretic. This is the clinical correlate of impaired natriuresis that exists in most forms of experimental hypertension. Additionally, diuretics facilitate potassium excretion.

FOLLOW-UP

Section 8 of 11  

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Further Inpatient Care

• In-hospital care may be needed for complications, such as fluid overload or hyperkalemia.
• In the case of acute BMT nephropathy associated with a HUS- and/or TTP-like disorder, the use of plasma exchange may be considered. This treatment may reverse the hematologic component, but it does not improve renal function (Sarode, 1995).
• With any patient with chronic renal disease, intercurrent illness may precipitate hospitalization.
• • Most patients with renal insufficiency require a dose adjustment for many medications. Avoid the use of any nephrotoxic medications, such as nonsteroidal anti-inflammatory drugs.
  • Should it become necessary to use intravenous radiocontrast, the use of intravenous isotonic sodium chloride solution to expand the volume in the patient reduces the risk of contrast nephrotoxicity.

Further Outpatient Care

• Outpatient care of any patient with chronic renal failure requires sufficient frequency of visits, attention to blood-pressure control, and assessment of the rate at which renal function is lost. These principles are valid for both radiation nephritis and BMT nephropathy.
• • Monthly or weekly outpatient visits may be needed for patients whose blood pressure remains uncontrolled or who have fluid overload requiring an adjustment of diuretic doses.
  • The rate of loss of kidney function is adequately assessed by construction of a graph of 100/plasma creatinine versus time. Such a graph should be updated after each visit. Such a graph may permit prediction of future decline in renal function and its timing.

In/Out Patient Meds

• ACE inhibitors, ARBs, and/or calcium channel blockers control blood pressure. Improved blood-pressure control helps to slow the progression of renal failure. In subjects with chronic kidney disease, especially when the serum creatinine level is elevated or the GFR is reduced, more than one antihypertensive drug is typically needed to control the blood pressure.
• Diuretics treat fluid overload and enhance potassium excretion.
• Erythropoietin treats anemia.
• Kayexalate treats hyperkalemia.
• Fludrocortisone treats aldosterone deficiency and hyperkalemia.

Transfer

• Transfer or referral may be necessary in the event of complications or management difficulty.

Deterrence/Prevention

• The use of ACE inhibitors (eg, captopril) may mitigate, or even entirely prevent, radiation nephritis if patients are started soon enough after the initial irradiation.
• This effect has been demonstrated in experimental animals, but clinical study is required before this treatment is used in humans.

Complications

• Fluid overload, edema, pulmonary edema
• Hyperkalemia
• HUS- and/or TTP-like syndrome
• Uremia with the need for dialysis

Prognosis

• Radiation nephritis may progress to end-stage renal failure. The same is true of its modern congener, BMT nephropathy, and has also occurred after internal radioisotope radiotherapy.
• • Complete renal failure may evolve in weeks in severe cases, years in less severe cases.
  • Predict when a patient will need dialysis by using a 100/plasma creatinine graph. At the point where the 100/plasma creatinine value is equal to 10, the estimated renal function is approximately 10% of normal, and dialysis may be needed soon.
• Patients with BMT nephropathy whose renal function declines to the point of their needing chronic dialysis have a poor prognosis compared with that of age-matched control subjects receiving dialysis. This probably is related to the burden of immunosuppression and past illness associated with BMT.
• Subjects with BMT nephropathy may have accelerated atherosclerosis, which may be related to total-body irradiation and chemotherapy (Akasheh, 1999).

Patient Education

• Any patient with chronic renal disease must comply with outpatient follow-up and blood-pressure control. This compliance helps to slow the decline in renal function; the same is true for radiation nephritis or BMT nephropathy.
• Patients must be aware of their maintenance medications and dosages. They must avoid nephrotoxins, such as over-the-counter nonsteroidal arthritis medicines, including ibuprofen.

MISCELLANEOUS

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• Miscellaneous
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Special Concerns

• Follow-up of patients who have received therapeutic irradiation must address not only the cancer for which they were irradiated but also possible injury to healthy tissue. For this reason, patients who have undergone BMT must have periodic medical visits.
• In addition, the use of new therapies involving radiation, such as radioisotope therapies, requires careful monitoring for unexpected injuries to healthy tissue. These injuries have occurred with the use of ⁹⁰Y-tagged somatostatin and ¹⁶⁶Ho-tagged phosphonate (Moll, 2001; Giralt, 2003).

MULTIMEDIA

Section 10 of 11  

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• Follow-up
• Miscellaneous
• Multimedia
• References

Media file 1:  Evolution of the glomerular filtration rate (GFR) versus time in a case of nephropathy related to bone marrow transplantation (BMT). GFR may be approximated as 100/plasm creatinine on the Y axis and graphed versus time on the X axis. As is true in many cases of BMT nephropathy, the evolution appears to be biphasic, with an initial rapid decline in GFR, then a slower plateau phase. The patient whose data are shown here ultimately underwent kidney transplantation.
	View Full Size Image
Media type:  Graph

Media file 2:  Photomicrograph of a kidney-biopsy sample in a case of nephropathy associated with bone marrow transplantation (periodic acid-Schiff stain). A glomerulus is in the center and is relatively hypocellular. Increased mesangial matrix is present. The glomerular basement membranes are thin; however, in some places, they are separated from the capillary lumens by a low-density matrixlike material. Interstitial fibrosis separates the tubules from each other. Arteriolar thickening and arteriolar hyalin both are present.
	View Full Size Image
Media type:  Photo

REFERENCES

Section 11 of 11

• Authors and Editors
• Introduction
• Clinical
• Differentials
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• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

• Akasheh M, Priyanath A, Pello N, et al. Accelerated atherosclerosis in a patient with post-BMT nephropathy. Bone Marrow Transplant. Jan 1999;23(2):199. [Medline].
• Choi KL, Bakris GL. Hypertension treatment guidelines: practical implications. Semin Nephrol. Jul 2005;25(4):198-209.
• Cohen EP, Lemann J Jr. The role of the laboratory in evaluation of kidney function. Clin Chem. Jun 1991;37(6):785-96. [Medline].
• Cohen EP, Piering WF, Kabler-Babbitt C, Moulder JE. End-stage renal disease (ESRD) after bone marrow transplantation: poor survival compared to other causes of ESRD. Nephron. Aug 1998;79(4):408-12. [Medline].
• Cohen EP. Radiation nephropathy after bone marrow transplantation. Kidney Int. Aug 2000;58(2):903-18. [Medline].
• Cohen EP, Moulder JE, Robbins ME. Radiation nephropathy caused by yttrium 90. Lancet. Sep 29 2001;358(9287):1102-3. [Medline].
• Cohen EP, Robbins ME. Radiation nephropathy. Semin Nephrol. Sep 2003;23(5):486-99.
• Cohen EP, Hussain S, Moulder JE. Successful treatment of radiation nephropathy with angiotensin II blockade. Int J Radiat Oncol Biol Phys. Jan 1 2003;55(1):190-3.
• Giralt S, Bensinger W, Goodman M, et al. 166Ho-DOTMP plus melphalan followed by peripheral blood stem cell transplantation in patients with multiple myeloma: results of two phase 1/2 trials. Blood. Oct 1 2003;102(7):2684-91. [Medline].
• Keane WF, Crosson JT, Staley NA, et al. Radiation-induced renal disease. A clinicopathologic study. Am J Med. Jan 1976;60(1):127-37. [Medline].
• Luxton RW. Radiation nephritis. A long-term study of 54 patients. Lancet. Dec 2 1961;2:1221-4. [Medline].
• Markowitz GS, Appel GB, Fine PL, et al. Collapsing focal segmental glomerulosclerosis following treatment with high-dose pamidronate. J Am Soc Nephrol. Jun 2001;12(6):1164-72. [Medline].
• Moll S, Nickeleit V, Mueller-Brand J, et al. A new cause of renal thrombotic microangiopathy: yttrium 90-DOTATOC internal radiotherapy. Am J Kidney Dis. Apr 2001;37(4):847-51. [Medline].
• Moulder JE, Fish BL, Cohen EP. Radiation nephropathy is treatable with an angiotensin converting enzyme inhibitor or an angiotensin II type-1 (AT1) receptor antagonist. Radiother Oncol. Mar 1998;46(3):307-15. [Medline].
• Sarode R, McFarland JG, Flomenberg N, et al. Therapeutic plasma exchange does not appear to be effective in the management of thrombotic thrombocytopenic purpura/hemolytic uremic syndrome following bone marrow transplantation. Bone Marrow Transplant. Aug 1995;16(2):271-5. [Medline].
• Shetty HB, Howat AJ, Anderton JG. ANCA +ve/anti-GBM +ve vasculitis following bone marrow transplantation. Nephrol Dial Transplant. Dec 2002;17(12):2280-1. [Medline]. [Full Text].
• Stevens LA, Coresh J, Greene T, Levey AS. Assessing kidney function--measured and estimated glomerular filtration rate. N Engl J Med. Jun 8 2006;354(23):2473-83.

Article Last Updated: Dec 8, 2006