Renal Biopsy Case History
March, 1995

Pathologic diagnosis:
Minimal Change Glomerulopathy with Acute Renal Failure Syndrome

Follow Up:

The lithium was discontinued and the patient was treated with prednisone (60 mg/day). Five days after biopsy his creatinine was 6.1 mg/dl, and was 1.1 mg/dl one month later, at which time there was 1 g/24 hrs proteinuria. Within two months the proteinuria had disappeared and the serum albumin was 3.6 g/dl.

Discussion of Case by Dr. Jennette

Minimal change glomerulopathy with acute renal failure syndrome is one of the most gratifying diagnoses that a renal pathologist can make because prior to biopsy the patients are often thought to have either rapidly progressive glomerulonephritis (if the rapid rise in creatinine is documented) or severe irreversible chronic glomerular disease (if the patient already has a very high creatinine when first seen). Minimal change glomerulopathy with acute renal failure has a very good prognosis because the nephrosis usually responds to steroid treatment and the renal failure almost always resolves (1).

The clinical presentation in this patient supported a number of differential diagnostic considerations. The rapid rise in creatinine, the hematuria and the proteinuria all suggested some aggressive form of glomerular disease, possibly crescentic glomerulonephritis. Although in adults in general, the most common cause for crescentic glomerulonephritis is ANCA-associated glomerulonephritis, in an African-American with an ANA titer of 1:320, aggressive lupus nephritis would be a consideration. The normal serum complement would detract from this possibility but not rule it out entirely. For those clinicians (rheumatologists more often than nephrologists) who feel that renal biopsy is unnecessary prior to immunosuppressive treatment in patients with clinical evidence for lupus nephritis, this patient illustrates that everyone with high titer ANA, hematuria, proteinuria and renal failure does not have lupus nephritis.

The nephrotic range proteinuria in this patient was evidence against tubulointerstitial nephritis or acute tubular necrosis alone as the basis for the renal failure. Nephrotic syndrome with acute renal failure can be caused by nonsteroidal anti-inflammatory drugs, which can produce concurrent minimal change glomerulopathy and hypersensitivity tubulointerstitial nephritis, but this patient did not have a history of NSAID use.

Given the biopsy findings, the lithium that this patient was taking was possibly the basis for both the positive ANA (2) and the minimal change glomerulopathy (3). Lithium-induced minimal change glomerulopathy often resolves following discontinuation of lithium treatment but may require corticosteroid therapy.

Minimal change glomerulopathy with acute renal failure syndrome occurs almost exclusively in adults rather than children. In patients with minimal change glomerulopathy, risk factors for acute renal failure are older age, elevated systolic blood pressure and more severe proteinuria (1). Histologically, patients who have minimal change glomerulopathy with acute renal failure usually have some degree of arteriosclerosis and usually have focal areas of tubular epithelial simplification. These structural changes in tubules are usually less pronounced than in the specimen from the patient under discussion, and are absent in about a third of patient with this syndrome.

The vast majority of patients with minimal change glomerulopathy with acute renal failure syndrome have recovery of function over a period of weeks to months. A minority of patients require dialysis, which is usually short-term but may last for up to five weeks. Improvement in renal function usually parallels correction of fluid overload, and typically begins before the proteinuria resolves.


References

1. Jennette JC, Falk RJ: Adult minimal change glomerulopathy with acute renal failure. Am J Kidney Diseases, 1990 Nov, 16(5):432-437

2. Ananth J, Johnson R, Kataria P, Vandewater S, Kamal M, Miller M: Immune dysfunctions in psychiatric patients. Psychiatr J Univ Ott, 1989 Nov, 14(4):542-6

3. Wood IK, Parmelee DX, Foreman JW: Lithium-induced nephrotic syndrome. Am J Psychiatry, 1989 Jan, 146(1):84-7


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Last Update -- March 31, 1995