Prevalence of hepatitis C in patients with idiopathic glomerulopathies in native and transplant kidneys.

Previous studies suggest that there is an association between hepatitis C (HCV) infection and glomerular diseases in native and transplanted kidneys. However, the data are controversial. To reexamine this issue, we determined the prevalence of serum anti-HCV antibodies in patients with glomerulopathies of native kidneys (n = 105) and in patients with acute and chronic transplant glomerulopathy (TxGN) (n = 62). Compared with a control group of patients with diabetic nephropathy (n = 37, 0% HCV+), the prevalence of HCV antibodies was significantly higher in patients with focal glomerulosclerosis (FGS) (4 of 32, 13%, P = 0.04 by chi-square), but not in patients with membranous nephropathy (MGN) (1 of 19, 5%) or in patients with membranoproliferative glomerulonephritis (MPGN) (2 of 17, 12%). All of the patients with positive HCV serology had histories of intravenous (IV) drug use. Thus, HCV serology was negative in all of the patients with native glomerulopathies without histories of IV drug use. Compared with a group of 105 transplant patients without TxGN (1.8% HCV+), the prevalence of HCV antibodies was significantly higher in patients with acute (A)TxGN (12 or 41: 29%. P = 0.0004) and in patients with chronic (C)TxGN (9 of 27: 33%. P = 0.0004). Compared with controls, patients with ATxGN also had a significantly higher prevalence of serum immunoglobulin (Ig) M antibodies to cytomegalovirus (CMV) (3% and 26% of patients, respectively, P = 0.0004). However, there were no statistical associations between HCV and CMV serologies. These results do not support the postulate that HCV infection is associated with idiopathic native glomerulopathies; instead, the data suggest that the presence of HCV positivity in these patients can be explained by the inclusion of patients with a history of IV drug use. In contrast, these studies demonstrate for the first time an association between HCV infection and transplant glomerulopathies.

Reversible acute renal failure as an atypical presentation of ischemic nephropathy.

Ischemic nephropathy (IN) is defined as a clinically significant reduction in glomerular filtration rate in patients with hemodynamically significant obstruction to renal artery flow in a solitary functioning kidney or with bilateral renal artery stenosis (RAS). Ischemic nephropathy typically has a subacute to chronic course that may lead to end-stage renal disease. Acute anuric renal failure, which occurs less commonly with IN, is usually associated with moderately severe hypertension and has been attributed to certain risk factors: angiotensin-converting enzyme inhibition, a reduction in blood pressure secondary to antihypertensives or volume contraction, and exposure to contrast media. We present a series of six patients with IN and acute, anuric renal failure without either moderately severe hypertension or the previously defined risk factors. Of these six patients, four had RAS in a solitary kidney and two were found by ultrasound to have disparity in kidney size and bilateral RAS. Within 1 week of surgery, three patients developed renal failure that did not involve the kidney(s) responsible for the anuria and thus mimicked postoperative acute renal failure. Creatinine levels pre-anuria (1.2 to 2.1 mg/dL), during renal failure (5.0 to 12.8 mg/dL), and postrecovery (1.6 to 2.8 mg/dL) showed recovery of renal function, with renal artery bypass in four patients (sustained at 1 year). Two patients refused surgery and are on chronic dialysis. Acute renal failure in IN may occur postoperatively or spontaneously, and emergent intervention (ultrasound, angiography, angioplasty, and/or surgery) in this setting may lead to the correction of RAS and preservation of renal function.