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Acute renal insufficiency is a common problem, yet one that is frequently reversible with proper diagnosis and treatment. Although it has been argued that a renal biopsy is not needed for diagnosis in most cases of acute renal failure in the elderly, other studies have shown frequent disagreements between clinical and renal biopsy diagnoses in such cases. To investigate the causes of acute renal insufficiency in patients aged at least 60 years who underwent a renal biopsy and possible correlations between biopsy findings and renal survival, we first identified all native renal biopsy specimens from patients aged 60 years or older processed at The University of Chicago Medical Center (Chicago, IL) from 1991 through 1998 and reviewed the clinical records to determine the indication for the biopsy. We then reviewed again the records of those patients who underwent biopsy because of acute renal insufficiency, recorded the primary renal biopsy diagnosis in each of these cases, and obtained follow-up information for patients who underwent biopsy before July 1996. During the study period, 1,065 of 4,264 biopsy specimens (25.0%) received were obtained from patients aged 60 years or older, and acute renal insufficiency was the indication for biopsy in 259 of these patients (24.3%). The most frequent primary diagnoses on these latter biopsy specimens were pauci-immune crescentic glomerulonephritis (GN) with or without arteritis, 31.2% of biopsy specimens; acute interstitial nephritis, 18.6%; acute tubular necrosis (ATN) with nephrotic syndrome, 7.5%; atheroemboli, 7.1%; ATN alone, 6.7%; light chain cast nephropathy (LCCN), 5.9%; postinfectious GN, 5.5%; anti-glomerular basement membrane antibody nephritis, 4.0%; and immunoglobulin A (IgA) nephropathy and/or Henoch-Schönlein nephritis, 3.6%. Eight biopsy specimens (3.2%) showed only benign nephrosclerosis without an apparent cause of acute renal insufficiency, and another six specimens were inadequate. The renal biopsy diagnosis was in agreement with the prebiopsy clinical diagnosis (or differential diagnosis) in 107 of the 161 cases (67%) in which such information was provided. The distribution of diagnoses was similar in patients in the age groups of 60 to 69, 70 to 79, and 80 years or older, although younger age correlated significantly with improved renal and patient survival. The relative risk for progression to end-stage renal disease (ESRD) also increased according to diagnostic categories: LCCN (greatest risk) > GN other than pauci-immune > atheroemboli congruent with pauci-immune crescentic GN > tubulointerstitial diseases other than LCCN (the latter category including ATN with nephrotic syndrome). Development of ESRD correlated significantly with decreased patient survival. In summary, renal biopsy in patients aged 60 years or older with acute renal insufficiency uncovered the cause in greater than 90% of the cases and provided clinically useful information with respect to expectation for renal survival and potential treatment options.

Data compiled during the 1970s and early 1980s indicated that during these periods, membranous nephropathy was the most common cause of unexplained nephrotic syndrome in adults, followed in order of frequency by minimal-change nephropathy and focal segmental glomerulosclerosis (FSGS). However, we and others recently reported an increase in the incidence of FSGS over the past two decades, and the number of cases of FSGS diagnosed by renal biopsies in these centers now exceeds the number of cases of membranous nephropathy. Nonetheless, as a substantial fraction of patients with FSGS do not have the nephrotic syndrome, it remained unclear as to what extent the relative frequencies of FSGS and other glomerulopathies as causes of the nephrotic syndrome have changed over this time. To address this concern, we reviewed data from 1,000 adult native kidney biopsies performed between January 1976 and April 1979 and from 1,000 biopsies performed between January 1995 and January 1997, identified all cases with a full-blown nephrotic syndrome of unknown etiology at the time of biopsy, and compared the relative frequencies with which specific diseases were diagnosed in these latter cases between the two time intervals. The main findings of this study were that, first, during the 1976 to 1979 period, the relative frequencies of membranous (36%) and minimal-change (23%) nephropathies and of FSGS (15%) as causes of unexplained nephrotic syndrome were similar to those observed in previous studies during the 1970s and early 1980s. In contrast, from 1995 to 1997, FSGS was the most common cause of this syndrome, accounting for 35% of cases compared with 33% for membranous nephropathy. Second, during the 1995 to 1997 period, FSGS accounted for more than 50% of cases of unexplained nephrotic syndrome in black adults and for 67% of such cases in black adults younger than 45 years. Third, although the relative frequency of nephrotic syndrome due to FSGS was two to three times higher in black than in white patients during both study periods, the frequency of FSGS increased similarly among both racial groups from the earlier to the later period. Fourth, the frequency of minimal-change nephrotic syndrome decreased from the earlier to the later study period in both black and white adults. Fifth, the relative frequency of membranoproliferative glomerulonephritis as a cause of the nephrotic syndrome declined from the 1976 to 1979 period to the 1995 to 1997 period, whereas that of immunoglobulin A nephropathy appeared to increase; the latter accounted for 14% of cases of unexplained nephrotic syndrome in white adults during the latter study period. Finally, 10% of nephrotic adults older than 44 years had AL amyloid nephropathy; none of these patients had multiple myeloma or a known paraprotein at the time of renal biopsy.

Studies and textbooks from the 1970s and early 1980s list focal-segmental glomerulosclerosis (FSGS) as accounting for 10% to 15% of cases of idiopathic nephrotic syndrome in adults, although a recent review by D'Agati (Kidney Int 46:1223-1241, 1994) reported an approximately sevenfold increase in the incidence of FSGS from 1974 to 1993 in an active renal biopsy practice. To investigate possible changes in the incidence of FSGS in our renal biopsy practice, we reviewed reports from all nontransplant, adult (> or = 18 years) renal biopsies received in our laboratory from 1974 to 1993, which comprised 7,420 cases. All diagnoses of membranous nephropathy (MN), minimal change nephropathy (MCN), and FSGS made in each year were compiled; cases clearly or suspicious of being secondary to an underlying systemic disease, glomerulonephritis, or drug reaction were excluded. Relative frequencies of MN, MCN, and FSGS among these three diseases and among all biopsies were calculated for each year of the study. Regression analysis showed a significant (P < 0.001) increase in the odds of a diagnosis of FSGS over the study period: 7.6% per year among all biopsies and 6.8% per year among cases of MN, MCN, and FSGS only. Among all biopsies, the yearly incidence of FSGS increased from 4.0% +/- 0.6% (mean +/- SD) during the period between 1974 and 1979 to 12.2% +/- 2.0% during the period from 1987 to 1993. The odds of a diagnosis of MN (mean yearly incidence, 9.5% +/- 1.9%) did not vary significantly over the study period while the odds of a diagnosis of MCN (mean yearly incidence, 4.0% +/- 1.2%) declined at a rate of 2.2% per year (P < 0.03). Frequencies of diagnosis of MN, MCN, and FSGS by two pathologists were almost identical. Review of available slides from cases of FSGS revealed 21 (none before 1980) with characteristic histologic features of the collapsing glomerulopathy (CG) variant of FSGS. No more than four cases of CG were observed in any year of the study, and CG accounted for 4.7% of total FSGS cases for which diagnostic slides were available. Compared with 42 patients with non-CG FSGS, the CG cohort showed a greater percentage of black patients (86% v 38%), significantly higher mean levels of serum creatinine (3.8 +/- 2.7 mg/dL v 1.9 +/- 1.5 mg/dL) and urinary protein (14.3 +/- 9.6 g/24 hr v 7.7 +/- 5.8 g/24 hr) at the time of renal biopsy, and a greater likelihood of and more rapid progression to end-stage renal failure.(ABSTRACT TRUNCATED AT 400 WORDS)

Kidney failure is recognized to occur in association with bone malformations, yet the renal disease often is incompletely characterized. In the syndrome of cone-shaped epiphyses of the phalanges and renal failure (conorenal syndrome), the kidney disease has been previously labeled "nephronophthisis" (now termed "medullary cystic disease"). We report two siblings with the conorenal syndrome in whom longitudinal clinical study has been possible and from whom kidney biopsy specimens were obtained prior to renal failure; their renal disease is incompatible with medullary cystic disease. The variable clinical course and nephropathology of this syndrome are characterized. These results call into question the association of medullary cystic disease of the kidney with other syndromes of bone dysplasia with renal failure.

We describe the first reported case of a renal transplant patient who had two consecutive recurrences of membranous glomerulopathy in his allografts. Both recurrences were detected 1 year posttransplant. The first transplanted kidney was a none of six antigen match and his second was a four of six antigen match. The patient required a second kidney transplantation within 2 years of detection of the first recurrence. The second allograft has functioned adequately for nearly 4 years after diagnosis. The case and literature review illustrate that membranous glomerulopathy can recur in both poorly and well-matched allografts, that recurrence does not always occur faster in the better-matched kidneys, that cyclosporine does not prevent recurrent disease, and that the course of recurrent membranous glomerulopathy is unpredictable.

A comparative study was made using renal biopsy specimens obtained from US and Korean patients with lupus nephropathy. Significant differences were observed in the morphologic distribution and activity of the disease. Korean patients exhibited a higher frequency of World Health Organization class IV lupus nephropathy (77.8%) than black (47.2%) or white (42.1%) US patients (P less than 0.025, P less than 0.05, respectively), and a higher inflammatory intensity index (P less than 0.045) than US patients. Korean patients also showed a significantly lower frequency of WHO class III nephropathy (P less than 0.05). No significant morphologic differences were seen between the US white and black patient populations. These data suggest that the Korean patients had a more active and potentially more fulminating disease than the US patients. Whether differences in genetic and external causative factors play a role in the observed differences in renal histopathology among these groups remains to be clarified.

The morphologic alterations of true preeclampsia are well described and distinct. Using available criteria to define reversible pregnancy-induced nephropathy (PIN), the pathologist can offer the clinician information useful in predicting remote renal function and hypertension. True PIN is a usually completely reversible lesion in the nullipara and carries little risk of future hypertension. Nephrosclerotic vascular lesions, however, whether arteriolar, interlobular, or glomerular and resembling focal segmental glomerulosclerosis (FSGS), signify underlying hypertensive disease. This review summarizes information concerning the nature of PIN and also surveys 20 biopsies in women who mainly had severe preeclampsia, often with persistent postpartum hypertension. This material was step-sectioned and specifically reviewed in an effort to find FSGS in women with PIN.

We have previously described (Medicine 56:493, 1977) 12 patients with diffuse lupus glomerulonephritis who had no clinical or laboratory evidence of renal involvement at the time of the initial biopsy. In this article we report the course of 10 of these patients followed for 5-11 yr (mean 83 mo). One patient died in renal failure and two others of related causes (septicemia and subarachnoid hemorrhage). Seven patients (Group I) had a benign course from a renal standpoint, with stable renal function and mild or no urinary abnormalities. Repeat biopsy in four patients in this group revealed near complete resolution of the original lesion in two and considerable improvement in two others, who now have primarily mesangial hypercellularity and a focal lesion, respectively. Renal function deteriorated in three patients (Group II), resulting in loss of congruent to 50% of GFR in two and renal death in the third. Repeat biopsy in one of these patients showed a more severe, albeit focal, glomerulonephritis. Prognosis for renal function appears better in patients with silent nephropathy, but larger numbers are required to substantiate this impression. Until definitive answers become available, we believe it prudent to biopsy SLE patients even in the absence of overt renal involvement and to treat those with diffuse proliferative glomerulonephritis.

Unlike primary idiopathic childhood hemolytic uremic syndrome (HUS), certain cases of HUS are clearly secondary. This article describes a child who represents the 11th reported case of secondary HUS following bone marrow transplantation, and notably, the fourth such case without exposure to cyclosporine A. The renal biopsy was diagnostic in this case. Therefore, the pathognomonic features of the biopsy, as well as its prognostic implications are described and clarified. This patient was treated with plasma exchange, and is the second reported surviving case of secondary HUS following bone marrow transplantation.