Renal failure secondary to sarcoidosis.
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Biomedical subjects
Publications and source records attributed to K A Duncan.
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We studied the filtration characteristics of glomeruli isolated from the superficial and deep renal cortex of Munich-Wistar rats (180 to 300 gm) to determine whether the ultrafiltration coefficient (Kf) or hydraulic conductivity (Lp) of the glomerular capillary is altered during expansion of extracellular fluid volume with isotonic protein-free (SAL) or hyperoncotic (ALB) solutions. SAL rats were given an initial infusion of 1% dextrose in lactated Ringer's solution (0.1 ml/gm body weight) followed by a maintenance infusion for 18 to 20 hours. ALB rats were given hyperoncotic bovine serum albumin (0.01 gm/gm body weight) intravenously 2 hours before sacrifice. At sacrifice, urine flow rate and fractional excretion of sodium were increased and plasma renin activity decreased in both SAL and ALB rats. Expansion of intravascular volume was evidenced by a decrease in the hematocrit of ALB but not of SAL rats; plasma protein concentration was increased in ALB and unchanged in SAL rats. Kf and Lp were estimated during in vitro filtration. Because SAL rats were significantly larger than ALB rats, results were compared with those in separate size-matched controls. Kf of superficial glomeruli of large control and SAL rats did not differ (3.7 +/- 0.4 and 3.5 +/- 0.4 nl/min/mm Hg, respectively). Lp, of the same glomeruli, calculated as the quotient of Kf and estimated filtering area (LpD), were also comparable (1.9 +/- 0.2 and 1.8 +/- 0.2 microliter/min/mm Hg/cm2). Kf of superficial glomeruli of ALB rats was significantly greater than Kf of size-matched control rats (3.7 +/- 0.3 vs. 2.9 +/- 0.1 nl/min/mm Hg, P less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)
Urinary doubly refractile lipid bodies (oval fat bodies) are observed most frequently in patients with heavy proteinuria resulting from glomerular disease. We observed doubly refractile lipid bodies (DRLB) in the urine sediment of 60% of 35 patients with autosomal dominant polycystic kidney disease (ADPKD). All patients had clinical courses typical of ADPKD, and none exhibited the features of a second, unrelated renal disease. DRLB in the urine were correlated with a urine dipstick protein reading exceeding trace. Age, sex, BP, and serum creatinine concentration were not associated with the presence of DRLB in the urine. Examination of cyst fluid obtained from kidneys of six ADPKD patients revealed DRLB in 80% of cyst fluid samples that contained degraded blood (so-called chocolate cysts). The DRLB in cyst fluid were morphologically indistinguishable from those observed in urine, and DRLB from both sources were stained with oil red O. We conclude that urinary DRLB are a clinical feature of ADPKD.
The fibrinolytic enzyme streptokinase (streptase) was infused into the peritoneal catheter in 19 episodes of catheter failure in 16 patients. Intraabdominal bleeding prior to infusion was seen in seven of these episodes. Fibrin strands and clots were present in four additional successful cases. Streptokinase successfully relieved the obstruction in 13 episodes in 11 patients. The procedure failed in two cases of omental ingrowth and in another with catheter malposition. Streptokinase infusion also failed in two patients with Pseudomonas aeruginosa and one patient with Staphylococcus epidermidis peritonitis. Intraperitoneal streptokinase infusion is simple and free of side effects. Its use should be considered in peritoneal catheter failure, particularly in cases where bleeding or fibrin accumulation may play a role.
The pronounced leukopenia caused by cuprophane dialyzer membranes was significantly blunted by citrate regional anticoagulation. Cellulose acetate produced less leukopenia than the cuprophane, regardless of anticoagulant. The pO2 response to the initiation of hemodialysis was not affected by dialyzer membrane or anticoagulant choice. We therefore conclude that citrate anticoagulation reduces dialyzer-induced leukopenia. Citrate anticoagulation does not, however, change the hypoxemia present with acetate dialysis. The dissociation of leukopenia and hypoxemia with citrate anticoagulation suggests that pulmonary sequestration is not a major cause of hypoxemia during hemodialysis.
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