Severe hypernatremia complicating urinary tract obstruction.

Severe hypernatremia and hyperosmolar dehydration developed in a patient with partial urinary tract obstruction. The urine was initially hypotonic, and there was no response to exogenous vasopressin. These abnormalities resolved with relief of the urinary tract obstruction and replacement of the water deficit. This case documents lower urinary tract obstruction as a cause of nephrogenic diabetes insipidus and severe hypernatremia and illustrates its reversible nature.

Thrombotic thrombocytopenic purpura after a dogbite.

A man bitten by a pet dog had fulminant thrombotic thrombocytopenic purpura within 72 hours. Rhabdomyolysis was severe and acute anuric renal failure was present. The suspected causative agent was Pastuerella multocida or clostridia with possible endotoxemia, though early treatment precluded a definitive diagnosis. The patient responded dramatically to a combined therapeutic approach of antibiotics, steroids, splenectomy, and supportive hemodialysis.

Proliferative glomerulonephritis with crescent formation in behcet's syndrome.

Behcet's syndrome is a multisystem disease complex, the major manifestions of which are oral and genital ulcers, arthritis, uveitis, and skin eruptions. Less frequently, CNS disturbances, colitis, thrombophlebitis, large-vessel vaculitis, and myocarditis occur. If renal involvement does occur, it is usually manifested by asymptomatic microhematuria and/or proteinuria. Recently, renal amyloidosis and focal necrotizing glomerulonephritis with immune complex deposition have been described. We describe a patient with Behcet's syndrome who experienced diffuse proliferative glomerulonephritis with epithelial cell crescent formation in 75% of glomeruli examined. Immune complexes were not identified. Renal function, impaired on admission, improved with no therapy.

Reversible acute renal failure secondary to acute pyelonephritis.

We have described a case of reversible acute renal failure caused by acute pyelonephritis. In this entity, the kidneys are swollen by an interstitial infiltrate and edema, and white cell tubular casts and microabscesses may be present. Fractional excretion of sodium is high, and nephrotic proteinuria may occur without glomerular abnormalities. Recovery of renal function may occur if antibiotics are promptly instituted. Renal size generally decreases after recovery.

Thyroid antigen associated immune complex glomerulonephritis in Graves' disease.

A 60 year old hyperthyroid black woman with long-standing Graves' disease treated with methimazole presented with anasarca and congestive heart failure. She was found to have the nephrotic syndrome with a urinary protein excretion of 32 g/day. Light and electron microscopy revealed a stage II membranous glomerulopathy. Direct and indirect immunofluorescence demonstrated immunoglobulin G (IgG), immunoglobulin M (IgM), third component of complement and thyroglobulin in a granular diffuse pattern consistent with an immune complex glomerulonephritis. Total thyroidectomy led to a decrease in proteinuria with little change in glomerular filtration rate during an 11 month follow-up period. We believe this to be the first report of immune complex glomerulonephritis associated with thyroid antigen in Graves' disease.

Obstruction of the inferior vena cava complicating hemodialysis in polycystic kidney disease.

Two patients with polycystic kidney disease and renal failure developed profound hypotension within 30 minutes after starting hemodialysis. After ruling out all recognized causes of hypotension during early dialysis, we found that their vena cavas were obstructed by compression of the vessels against the spinal column by the greatly enlarged polycystic kidneys. Immediately after bilateral nephrectomy, the patients had dialysis, with removal of large amounts of fluid without causing hypotension. We speculate that compression of the vena cava by massively enlarged polycystic kidneys may significantly contribute to the renal insufficiency by greatly increasing renal venous pressure.

Hemodialysis of theophylline in uremic patients.

Hemodialysis of theophylline was studied in three uremic patients. The dialysis clearance ranged from 75.6 to 97.9 ml/min and averaged 88.1 ml/min. A much smaller value of 32.8 ml/min was reported by Levy and associates. The difference may be attributed to the two monitoring factors during hemodialysis, namely, blood and dialyzate flow rates. Both were higher in our study. Analysis of the semilogarithmic plots of the arterial plasma concentration versus time over a 3-hour period gave apparent half-lives of 3.15, 2.04, and 2.73 hours, respectively, for the three patients. Half-life of theophylline in normal subjects ranged from 4 to 6 hours or even longer. A prolonged half-life of theophylline in uremia could be expected. Our kinetic study indicated an approximately 50 per cent reduction in terminal half-life during hemodialysis. Hourly dialyzate was collected from one patient to account for drug recovery in the dialysis fluid. Forty per cent of the administered dose was recovered in the dialyzate during a 3-hour dialysis period, indicating effective removal. Dialysis clearance for creatinine was calculated by arterial-venous difference and correlated with that of theophylline. We found that theophylline was cleared by the dialyzer at a rate approximating 63 per cent of creatinine removal.

Fibrolipomatosis of the transplanted kidney.

Fibrolipomatosis of varying degree was observed in 24 transplanted kidneys. In 8 patients there was no history of urinary tract obstruction or multiple infections, leaving earlier rejection periods as the probable factor responsible for development of fibrolipomatosis after transplantation.

Severe diarrhea secondary to propranolol.

We have described two patients with propranolol-induced severe diarrhea, confirmed by rechallenge with the drug. In both cases the diarrhea was readily reversible with discontinuation of the drug.

Reversible depression in myocardial performance in dogs with experimental phosphorus deficiency.

The effects of phosphorus depletion on cardiac muscle function in six awake dogs were evaluated with surgically implanted transducers to serially measure ascending aortic root blood flow and high fidelity left ventricular pressure. After the animals recovered from surgery, phosphorus depletion was induced by feeding them a synthetic phosphorus-deficient diet plus aluminum carbonate gel for 35 days, followed by the same diet with phosphorus supplementation for 21 days. In addition to the cardiac studies, sequential measurements of phosphorus content in skeletal muscle and phosphorus in serum were obtained to ascertain the level of phosphorus depletion. Serum inorganic phosphorus concentration (mg/100 ml) decreased from 5.1 +/- 0.1 on day 0 to 0.9 +/- 0.1 on day 35 (P less than 0.01), and total muscle phosphorus (content mmul/100 g fat-free dry weight) decreased from 28.0 +/- on day 0 to 22.6 +/- 0.5 on day 35 (P less than 0.01). During the period of phosphorus depletion, there was no significant change in heart rate; however, stroke volume (milliliter) and peak blood flow velocity (centimeter per second) declined from 24 +/- 2 to 17 +/- 2 (P less than 0.01) and 121 +/- 12 to 98 +/- 7 (P less than 0.01), respectively. Maximum ascending aortic blood flow acceleration (centimeter per second square) and maximum left ventricular time rate of change of pressure (mm Hg per second) also decreased from 4,630 +/- 313 to 3,817 +/0 346 (P less than 0.01) and 2,582 +/- 347 to 2,120 +/- 297 (P less than 0.01) during phosphorus depletion. After repletion all values returned to control values. These results indicate that moderate diet-induced phosphorus depletion can depress myocardial performance. With repletion of phosphorus, myocardial performance improves.

Hypophosphatemia and rhabdomyolysis.

Clinical observations suggest that overt rhabdomyolysis may occur if severe hypophosphatemia is superimposed upon a pre-existing subclinical myopathy. To examine this possibility, a subclinical muscle cell injury was induced in 23 dogs by feeding them a phosphorus- and calorie-deficient diet until they lost 30% of their original weight. To induce acute, severe hypophosphatemia in the animals after partial starvation, 17 of the dogs were given large quantities of the same phosphorus-deficient diet in conjunction with an oral carbohydrate supplement, which together provided 140 kcal/kg per day. After phosphorus and caloric deprivation, serum phosphorus and creatine phosphokinase (CPK) activity were normal. Total muscle phosphorus content fell from 28.0+/-1.3 to 26.1+/-2.5 mmol/dg fat-free dry solids. Sodium, chloride, and water contents rose. These changes resembled those observed in patients with subclinical alcoholic myopathy. When studied after 3 days of hyperalimentation, the animals not receiving phosphorus showed weakness, tremulousness, and in some cases, seizures. Serum phosphorus fell, the average lowest value was 0.8 mg/dl (P <0.001). CPK activity rose from 66+/-357 to 695+/-1,288 IU/liter (P <0.001). Muscle phosphorus content fell further to 21.1+/-7.7 mmol/dg fat-free dry solids (P <0.001). Muscle Na and Cl contents became higher (P <0.01). Sections of gracilis muscle showed frank rhabdomyolysis.6 of the 23 phosphorus- and calorie-deprived dogs were also given 140 kal/kg per day but in addition, each received 147 mmol of elemental phosphorus. These dogs consumed their diet avidly and displayed no symptoms. They did not become hypophosphatemic, their CPK remained normal, and derangements of cellular Na, Cl, and H(2)O were rapidly corrected. The gracilis muscle appeared normal histologically in these animals. These data suggest that a subclinical myopathy may set the stage for rhabdomyolysis if acute, severe hypophosphatemia is superimposed. Neither acute hypophosphatemia nor rhabdomyolysis occur if abundant phosphorus is provided during hyperalimentation.

New method for obtaining uncontaminated urine from women.

Midstream sampling and colony counts have greatly improved precision in diagnosing urinary tract infections. In women, however, contamination by vaginal flora and cells still poses a diagnostic problem. We have devised an instrument for helping collect uncontaminated urine from women and have tested it in three sets of observations. Approximately 96% of 200 women were able to use the device successfully after minimal instruction. Bacterial colony counts and quantitative estimation of vaginal epithelial cells were performed on urine collected by 18 female volunteers using conventional clean-catch technics and on urine collected by the same 18 women using the Clean Streamer. The average bacterial colony count in conventionally collected urine was 8,100/ml while in Clean Streamer collected urine it was 1,722/ml. The average number of vaginal epithelial cells in conventionally collected urine was 22.4/ml while in Clean Streamer collected urine it was 14.1/ml. The difference in both comparisons is statistically significant (P = .01). We believe that use of the Clean Streamer greatly facilitates the ability of a woman to collect a urine sample uncontaminated by vaginal secretions and flora.

Severe hyperchloremic acidosis complicating jejunoileal bypass.

In summary, severe hyperchloremic acidosis developed in two patients as a late complication after jejunoileal bypass for morbid obesity. This acidosis was associated with episodes of dizziness, ataxia, headache, weakness, confusion and transient loss of consciousness. Recognition of this symptom complex in the patient with a jejunoileal bypass should suggest metabolic acidosis as a complication of this surgical procedure. Bicarbonate replacement provided prompt, but temporary, improvement in the symptoms and the acidosis. Revision of the intestinal bypass was required for correction. Special studies to rule out renal tubular acidosis were performed and definitely excluded the kidney as a source of the acidosis.

Listeria cerebritis: relapse of infection in renal transplant patients.

In 3 cases of Listeria cerebritis, two of the patients had relapse with cerebritis after antimicrobial therapy for acute Listeria septicemia or meningitis. Each had received ten to 14 days of intravenous penicillin. Relapse occurred with fever and sudden focal cerebral dysfunction. Brain scans showed focal uptake; arteriograms and computerized tomography were normal. Cerebrospinal fluids were nondiagnostic; blood cultures yielded Listeria in two patients. Penicillin treatment for six weeks produced rapid clinical responses that were complete in one and minimal residual in two. Progress brain scans were normal. A relapse rate of 35% is reported in transplant patients with Listeria meningitis and/or bacteremia who are treated for less than three weeks; to our knowledge, cerebritis in such patients has not been reported previously. High-dose penicillin or ampicillin therapy for four to six weeks is recommended for Listeria infections in this select group.