Piretanide: effective diuretic in renal failure.
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Biomedical subjects
Publications and source records attributed to C R George.
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Patients with chronic renal failure who received bolus doses of piperacillin maintained high serum levels for up to six hours. The percentage of the injected dose which was detectable in the urine in 24 hours was reduced proportionately to the severity of the renal failure.
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A 39-year-old man with a lifelong history of tetany and hypocalcaemia was found to have hypomagnesaemia (0.29 mmol/l) due to renal magnesium loss. His asymptomatic 29-year-old brother had a similar disorder. Both were infertile and had severe oligospermia but normal endocrine function. They had medullary nephrocalcinosis and glomerular filtration rate was reduced. Renal biopsy showed patchy interstitial fibrosis and some glomerular sclerosis. Electron microscopy showed thickened basement membranes in damaged glomeruli and in tubules in areas of fibrosis. Tests of renal tubule function were normal. Hypocalcaemia and tetany were corrected by oral magnesium supplements which raised the serum magnesium level to around 0.54 mmol/l.
Aspects of humoral and cellular immunity and of the complement system were examined in 44 patients with glomerulonephritis, and in control subjects. A number of patients with glomerulonephritis were shown to have evidence of altered immunity which may reflect underlying mechanisms of glomerular injury. Mesangial IgA glomerulonephritis was associated with elevation of serum IgA levels (P less than 0 . 001), and focal sclerosing glomerulonephritis with raised serum IgM (P less than 0 . 001). Serum IgG levels were abnormal in 15 patients with glomerulonephritis. The haemagglutinating antibody response to tetanus toxoid was reduced in patients compared with controls. Levels of serum complement components were increased, with some exceptions, and C-reactive protein levels were also significantly raised (P less than 0.001), findings consistent with an ongoing inflammatory process. No impairment in response to recall antigens or sensitisation to dinitrochlorobenzene was found, but phytohaemagglutinin induced lymphocyte transformation was reduced in some forms of the disease.
The BPs of 86 of 100 severely hypertensive patients were controlled by measures designed to reduce total body sodium, namely a low salt diet plus the addition of incrementally increased frusemide treatment if diet alone was inadequate. Control of hypertension was maintained over prolonged periods of time in 70 of the patients. Among the 14 who failed to respond adequately, mean plasma renin level was higher (when tested) than in those who did respond adequately, and renal artery stenosis was discovered in 2. Supplementary propranolol controlled the hypertension in 8 of the inadequate responders.
Bone biopsies from 37 haemodialysis patients were embedded in a methyl methacrylate:hydroxyethylmethacrylate mixture and consecutive sections taken for: (1) acid phosphatase activity (osteoclasts), (2) pyronin stain for RNA (osteoblasts), and (3) fluorescence for tetracycline. Images of the three sections were traced using a camera lucida and the tracing quantitated with a digitiser. Osteomalacia (OM) was diagnosed by increased osteoid with decreased tetracycline and hyperparathyroidism (HPT) by an increased osteoclast count. OM was present in 8 patients, HPT in 11, OM + HPT in 16, and no disease in 2. Biochemistry could not predict the histology. Histologically, though HPT could be satisfactorily diagnosed, problems still remain in the definition of OM, particularly when combined with HPT.
A pancreatic pseudocyst within the wall of the duodenum is presented. Its radiographic features were analyzed and comprehensively compared with 10 proved cases. These pseudocysts can be intramural or extrinsic severely compressive lesions. The occurrence of these pseudocysts at multiple sites throughout the gastrointestinal tract emphasizes the need to consider them in the differential diagnosis of severe extrinsic compressive or intramural lesions.
Mice were infected with 1X 107 Plasmodium berghei Yoelii parasites intraperitoneally. Circulating parasite, malaria antibody and C3 concentrations were measures: parasitaemia and hypocomplementaemia were transient, but the antibody response was persistent. Animals were sacrificed at intervals and their kidneys examined: a glomerulonephritis associates with predominantly mesangial deposits of C3, IgG1, IgM and some IgA always developed after 7 days and persisted for up to 6 mth. Malaria antigen and antibody were demonstrated within the glomeruli. Microscopic haematuria occurred with proteinuria but without marked deterioration in renal function. Strains producing high and low affinity antibody were equally susceptible to the disease. Treatment with glucocorticoid, immunosuppressive, platelet function inhibiting and/or anticoagulant drugs, or indomethacin from the 1st day of infection failed to prevent development of the disease or to lead to its early cure. Eradication of the infection within its first 3 days prevented glomerular deposition of antibody and complement, and infection with a smaller antigen load followed by later treatment also produced subsequent cure.
A twenty year old woman presented with pulmonary hemorrhage and glomerulonephritis with linear deposition of IgG on the glomerular capillary basement membrane, and high titer of antiglomerular basement membrane antibody in her serum. Without treatment, renal function, which was transiently impaired, has improved, pulmonary hemorrhage subsided, and repeat renal biopsies have revealed the appearance of nonlinear in addition to the linear deposition of IgG on the glomerular capillary basement membrane in the face of diminished serum antiglomerular basement membrane antibody titer.
18 children with clinical and laboratory findings characteristic of the hemolytic uremic syndrome were retrospectively studied. Thrombocytopenia due to platelet destruction was accompanied by only minimal changes in fibrinogen turnover and fibrinolytic degradation products. The most consistent pathologic feature was severe renal endothelial cell injury, which was postulated to produce both platelet and red cell destruction. Despite initially severe renal damage, 90% of the patients ultimately recovered normal renal function if adequately supported during the acute phase of the disease.
The clinical features and renal histology of twelve chinldren who developed nephrotic syndrome in the first year of life were studied. Six suffered from microcystic disease and six from primary mesangial cell proliferation and/or sclerosis. A consistent family history, premature birth, large placenta pressence of other congenital abnormalities, onset in the first two months of life and lower plasma albumin level all suggested microcyste disease, but the most reliable distinction was histological. All microcystic children died within two years, whereas four with primary mesangial disease survived indefinitely. Corticosterid and immunosuppressive herapy failed to help either group and most deaths were due to sepsis, especialy with E. coli.
Serial studies of platelet and fibrinogen survival were performed in 26 nonimmunosuppressed dogs after allogenic renal transplant operations. Treatment with acetylsalicylic acid, dipyridamole, and heparin failed to improve the selective platelet destruction which occurred in untreated animals, and it did not improve postoperative longevity. There was a high incidence of postoperative wound and intrarenal hemorrhage after heparin treatment. These results are consistent with the hypothesis that platelet destruction is a consequence rather than the cause of acute graft rejection, and it is concluded that antithrombotic therapy is not of practical benefit in preventing acute rejection.
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