Severe intimal hyperplasia with ischaemic colitis in two patients with hepatitis C.

Many extrahepatic manifestations of hepatitis C have been described, including renal disease and vasculitis. We describe the novel finding of intimal hyperplasia associated with severe ischaemic events in two patients with hepatitis C. The combination of genotype 1a hepatitis C virus, rapidly progressive mesangiocapillary glomerulonephritis and intimal hyperplasia with ischaemic sequelae, may represent a new syndrome.

Quinidine-induced allergic granulomatous angiitis: an unusual cause of acute renal failure.

A case of systemic allergic-type vasculitis after the administration of quinidine and digoxin is described. The renal biopsy findings are unique in that they describe an arteritis with eosinophilic infiltration and non-caseating granulomata. We believe quinidine is the antigen that was responsible for the reported findings.

Evidence for electroneutral sodium chloride transport in rat proximal convoluted tubule.

One- to two-thirds of NaCl absorption in the late proximal convoluted tubule (no luminal organic solutes present) is inhibited by cyanide and thus is dependent on active transport. To examine whether this active transport-dependent NaCl transport is electrogenic or electroneutral, the effect of cyanide on transepithelial potential difference (PD) was measured in the rat proximal convoluted tubule microperfused in vivo. In the presence of an ultrafiltrate-like luminal perfusate containing glucose and alanine, cyanide addition caused the transepithelial PD to change from -0.44 +/- 0.04 to -0.05 +/- 0.03 mV (P less than 0.001). In the presence of a late proximal tubular fluid (high chloride, low bicarbonate, no organics), the transepithelial PD was 1.23 +/- 0.06 mV and was unchanged at 1.19 +/- 0.05 mV after cyanide addition (NS). To eliminate the possibility that an effect of cyanide on a putative acidification-dependent lumen-positive PD was concealing an effect on an electrogenic sodium transport-dependent lumen-negative PD, the above studies were repeated in the presence of acetazolamide. Cyanide did not affect the transepithelial PD (1.17 +/- 0.05 vs. 1.07 +/- 0.06 mV, NS). We conclude that, although cyanide-inhibitable NaCl transport is electrogenic in the presence of luminal organic solutes, it does not generate a transepithelial PD in their absence and therefore is electroneutral.

Active and passive components of chloride transport in the rat proximal convoluted tubule.

Rat proximal convoluted tubules were perfused in vivo to examine the active and passive components of chloride absorption. Chloride flux was a linear function of the transepithelial electrochemical driving force, yielding a permeability coefficient of 20.6 X 10(-5) cm/s. In the absence of an electrochemical driving force, chloride absorption persisted at the rate of 131 peq/mm X min, thus demonstrating active absorption of chloride. Addition of luminal cyanide to tubules absorbing chloride inhibited net chloride absorption. In tubules perfused with a low luminal chloride concentration in which there was net chloride secretion, addition of luminal cyanide increased the magnitude of net chloride secretion. These studies demonstrate that transepithelial chloride transport involves two components: a passive paracellular flux and an active transcellular flux. Cyanide affects net chloride flux by inhibiting active transcellular chloride absorption.

Amiloride inhibition of proximal tubular acidification.

In brush border membrane vesicles prepared from mammalian kidney cortex, amiloride is a potent inhibitor of the Na+/H+ exchanger. In the present study, in vivo microperfusion was used to examine the effect of luminal amiloride on transport in the rat superficial proximal convoluted tubule. At a perfusion rate of 14 nl/min, addition of 10(-3) M amiloride to artificial early proximal tubular fluid reduced bicarbonate absorption from 103 +/- 7 to 81 +/- 5 pmol mm-1 X min-1 and volume absorption from 2.03 +/- 0.15 to 1.57 +/- 0.06 nl X mm-1 X min-1. Glucose efflux was unchanged, excluding nonspecific inhibition of Na+-K+-ATPase. Luminal amiloride at 10(-4) M did not affect bicarbonate absorption or volume absorption. At a perfusion rate of 41 nl/min, 10(-3) M amiloride reduced bicarbonate absorption from 179 +/- 8 to 114 +/- 9 pmol X mm-1 X min-1, a significantly greater inhibition than that seen in tubules perfused at 14 nl/min. Amiloride at 10(-3) M had no significant effect on sodium chloride absorption as measured by volume flux from an artificial late proximal tubular fluid. The results show that luminal amiloride specifically inhibits proximal acidification and demonstrate involvement of the Na+/H+ antiporter in proximal tubular acidification. However, the inhibition of acidification is less than the inhibition of Na+/H+ exchange predicted by vesicle studies.