Dialysate protein losses with bleach processed polysulphone dialyzers.

We measured dialysate protein losses from polysulphone dialyzers undergoing repetitive processing with bleach and formaldehyde. The entire dialysate was collected during the first, fifth and tenth use of F-80 dialyzers. Dialysate protein concentration was 1.5 +/- 0.4 mg/dl N = 11 +/- SEM) during the first use, 2.1 +/- 0.3 mg/dl during the fifth use and 3.6 +/- 0.5 mg/dl (N = 10) during the tenth use. In a follow-up study, dialyzers were evaluated for up to 25 uses. After 12 to 15 uses dialysate protein was 7.9 +/- 0.8 mg/dl (N = 13), after 16 to 20 uses; 12.0 +/- 1.2 mg/dl (N = 13) and after 23 to 25 uses; 19.9 +/- 2.1 mg/dl (N = 5). Mean dialysate volume was 83.9 +/- 1.1 liters (N = 63) yielding total protein losses of up to 20.7 grams per treatment. Dialysate albumin losses, which were unmeasurable during the first use of the dialyzers, revealed a similar increase with reuse resulting in a mean value of 14.4 +/- 3.2 mg/dl after 23 to 25 reuses (N = 5). Dialysate beta-2 microglobulin (beta 2m) levels were 1.05 +/- 0.13 mg/l for dialyzers bleached < 10 times (N = 32) versus 1.54 +/- 0.15 mg/liter for dialyzers bleached > 10 times (N = 31, P < 0.02 vs. < 10 reuses). A random sampling of dialyzers processed without bleach for 8, 14, 15, 24 and 25 reuses revealed minimal protein losses, ranging from 1.4 to 2.7 mg/dl with no relation to reuse number and no measureable albumin.(ABSTRACT TRUNCATED AT 250 WORDS)

Mesangial proliferative glomerulonephritis with IgM deposits. Clinicopathologic analysis and evidence for morphologic transitions.

To determine the natural history of mesangial proliferative glomerulonephritis (MesPGN) with IgM deposits and its relationship to minimal change disease (MC) and focal segmental glomerulosclerosis (FGS), we studied the clinical characteristics and outcome in 20 patients with MesPGN, 8 with MC, and 10 with FGS. IgM deposits were present in glomeruli of all MesPGN patients. Progression to FGS was documented in 2 patients with MesPGN, 1 of whom developed renal failure. Transition from MC to MesPGN occurred in 1 patient. 2 MC patients developed FGS, with decline in renal function in 1 of them. These data suggest the possibility of histologic transition from MC to FGS directly or through the stage of MesPGN.

Metoprolol and alopecia.

Beta-adrenoceptor antagonists are very popular agents in the treatment of hypertension. Reversible alopecia of the telogen effluvium variety has been described with propranolol (inderal). We describe a case of reversible alopecia with metoprolol (Lopressor) which also was associated with a telogen effluvium on scalp biopsy, suggesting a similar mechanism for the alopecia associated with these agents.

Effect of gentamicin on p - aminohippurate metabolism and transport in rat kidney slices.

The mechanism by which gentamicin augments the uptake of p-aminohippurate (PAH) by rat renal cortical slices was investigated. In all experiments, gentamicin was administered as gentamicin sulfate at 100 mg/kg b.wt. per day for 2 days; control rats were injected with saline. The effect of gentamicin on the metabolism of PAH to p-aminobenzoic acid (PABA), acetyl-PABA and acetyl-PAH was studied by high performance liquid chromatography. No metabolites of PAH were detected in renal slices of gentamicin-injected or control rats incubated in medium containing PAH. Efflux of 14C-PAH was measured after incubating renal cortical slices for 2 hours in medium containing 8 X 10(-5) M 14C-PAH. The efflux rate constant was 0.080 +/- 0.003/min in control slices and 0.059 +/- 0.003/min in gentamicin slices, P less than .001. No significant difference in the diffusible pool of PAH was found between the two groups which supports an argument against increased tissue-binding of PAH as the explanation for the augmented uptake of PAH by slices of gentamicin-injected rats. Active PAH transport was assessed in terms of Michaelis-Menten kinetics. Vmax was 0.93 +/- 0.08 micronmol/g/15 min in control slices and 1.37 +/- 0.10 micronmol/g/15 min in gentamicin slices (P less than .005). The apparent reaction rate constant (Km) was not different; Km was 0.25 +/- 0.03 and 0.29 +/- 0.04 mM in control and gentamicin slices, respectively (P less than .4). In contrast to PAH, gentamicin did not alter uptake of N'-methynicotinamide, an organic base; nor did it alter the efflux rate constant or diffusible pool of N'-methylnicotinamide. Increased PAH uptake was still evident when slices of gentamicin-injected rats were incubated in medium without acetate. These studies indicate that gentamicin stimulates active PAH transport and decreases PAH efflux in rat renal cortical slices. Both changes implicate an effect of gentamicin at the antiluminal membrane of proximal tubular cells. The finding of an increase in Vmax without a change in Km raises the possibility that gentamicin increases the amount or availability of carrier protein-mediating PAH transport.

Effect of gentamicin on renal function in the rat.

The functional correlates of gentamicin nephrotoxicity were studied in rats injected with gentamicin, 100 mg/kg b.wt. per day, for 1 to 6 days. After 4 days of injections, a significant decrease in urine osmolality was detected in association with a rise in blood urea nitrogen and serum creatinine. These changes became more pronounced after 5 days of injections. Injecting gentamicin for 3 to 5 days had no discernible effect on the capacity of the distal nephron to reabsorb solute free water during a saline load compared to the control group. Tubular secretion of para-aminohippurate (PAH) was significantly greater in rats injected with gentamicin for 4 to 5 days than in the control group. Increased uptake of PAH by renal cortical slices was detected after 1 day of gentamicin treatment and reached a peak effect after 5 days of injections. Probenecid completely inhibited the augmented PAH uptake. No stimulation of the organic base transport system was observed. Three days of gentamicin treatment did not alter intracellular water or electrolyte content of kidney cortical slices. The data suggest that gentamicin specifically stimulates the organic acid transport system and that this effect may represent an early functional correlate of gentamicin nephrotoxicity.