ABSTRACT
A 22-year-old man with a ventriculojugular shunt had edema, hematuria, proteinuria, hypocomplementemia, azotemia, and S epidermidis bacteremia. Initial percutaneous renal biopsy showed a diffuse proliferative glomerulonephritis. Subendothelial and intramembranous deposits were seen on electron microscopy. Immunofluorescent studies were positive for IgG and C3. A repeat percutaneous renal biopsy six weeks after cessation of antibiotic therapy revealed a mild proliferative glomerulonephritis with some evidence of resolution. No deposits were seen on electron microscopy and immunofluorescent studies were negative. At elective shunt revision three months after cessation of therapy, culture of the jugular portion of the removed shunt revealed S epidermidis. Early recognition of immune complex glomerulonephritis occurring with an infected ventriculovascular shunt should permit early treatment (antibiotic therapy and removal of the infected foreign body) and a favorable outcome.
Subject(s)
Cerebrospinal Fluid Shunts/adverse effects , Glomerulonephritis/etiology , Immune Complex Diseases/etiology , Staphylococcal Infections , Adult , Complement C3 , Glomerulonephritis/immunology , Glomerulonephritis/pathology , Glomerulonephritis/therapy , Humans , Immune Complex Diseases/immunology , Immune Complex Diseases/pathology , Immune Complex Diseases/therapy , Immunoglobulin G , MaleABSTRACT
A patient with Bartter's syndrome in whom the disease was recognized at 52 years of age is described. Studies of his renal function suggest that the basic pathophysiologic defect was an abnormality in proximal tubular sodium reabsorption which led to extracellular fluid volume depletion and consequent stimulation of the renin-angiotensin-aldosterone axis. After comparing the physiologic studies in this patient with those in other reported cases, we postulate that Bartter's syndrome may represent the end result of different pathophysiologic processes which share in common juxtaglomerular hyperplasia, increased renin release and secondary hyperaldosteronism. Therapy with B-adrenergic blocking agents produced adverse effects, but the patient responded well to more conventional measures.
Subject(s)
Bartter Syndrome/diagnosis , Hyperaldosteronism/diagnosis , Kidney Tubules, Proximal/physiopathology , Bartter Syndrome/drug therapy , Bartter Syndrome/physiopathology , Extracellular Space , Humans , Hypokalemia/diagnosis , Hypotension/chemically induced , Male , Middle Aged , Natriuresis , Propranolol/adverse effects , Propranolol/therapeutic use , Renin/blood , Sodium/metabolismABSTRACT
Urinary excretion of sodium and water was investigated in patients with chronic end-stage renal disease before and after three different experimental manipulations: reduction in urea solute load by dialysis while extracellular fluid volume (ECFV) was maintained, dialysis without alteration in urea solute load or ECFV and reduction in ECFV without alteration in urea solute load. Sodium and water excretion significantly declined in association with a reduction in both urea solute load and ECFV, but not during a dialysis when reduction on both of these indexes was prevented. The excretory changes occurred in the absence of any alteration in creatinine clearance. The studies suggest that both solute load and the degree of extracellular fluid volume expansion contribute independently to the rate of sodium and water excretion in chronic renal disease. It is concluded that in any given patient the overall excretion of sodium and water is directly influenced by a number of factors including the solute load, the degree of ECFV and the glomerular filtration rate.
