Acute eosinophilic interstitial nephritis and sarcoidosis.
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Acute Disease↗
Biomedical subjects
M N Yum
Publications and source records attributed to M N Yum.
Interstitial nephritis caused by trimethoprim-sulfamethoxazole in renal transplant recipients.
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Bacteriuria↗
Comparative nephrotoxicities of dibekacin, amikacin, and gentamicin in a rat model.
The nephrotoxicity of dibekacin was compared with those of gentamicin and amikacin in a rat model. The doses used were 3, 10, and 30 times the suggested human therapeutic dose on a weight basis. Indices of glomerular and tubular function failed to clearly differentiate the drugs. Dibekacin and gentamicin produced equally severe injury to the renal tissue. Slightly less damage occurred with amikacin.
Amikacin↗
Childhood primary aldosteronism due to an adrenal adenoma: preoperative localization by adrenal vein catheterization.
Primary aldosteronism resulting from an adrenal adenoma is rare in children. An 8 1/2-year-old girl was found to have hypertension and spontaneous hypokalemia, both detected as incidental findings. Subsequent investigations revealed inappropriately elevated levels of plasma and urinary aldosterone with suppressed plasma renin activity. Adrenal vein blood sampling and venography suggested the presence of left adrenal adenoma which was confirmed at surgical exploration and pathologic examination. All the clinical and biochemical abnormalities were corrected by the adrenalectomy. The differential diagnoses of various types of hyperaldosteronism and/or hypokalemia in such a clinical setting are discussed.
Adenoma↗
Pseudolymphoma of the lung in a patient with systemic lupus erythematosus.
A 47 year old woman with systemic lupus erythematosus was found to have asymptomatic pulmonary nodules. Histologically they represented benign reactive lymphoreticular hyperplasia compatible with the diagnosis of pseudolymphoma. Immunofluorescence and electron microscopy demonstrated immunoreactants and electron-dense deposits in the alveolar and vascular walls, suggesting that an immune complex mechanism may be involved in this case.
Complement C3↗
Protection from gentamicin nephrotoxicity by cephalothin and carbenicillin.
In rats, cephalothin exerts a protective effect upon the nephrotoxicity of gentamicin. To examine the possibility that this effect is also observed with carbenicillin, we gave the following (milligrams per kilogram) to rats daily for 14 days: gentamicin alone, 60; gentamicin plus cephalothin, 100, 500, or 1,000; gentamicin plus carbenicillin, 50, 100, 250, 500, or 1,000. A 500-mg/kg dose of cephalothin afforded significant partial protection from gentamicin nephrotoxicity, as did a 100-mg/kg dose of carbenicillin. Increasing doses of either drug failed to increase protection. The data suggest that in rats not only does carbenicillin afford some protection from gentamicin nephrotoxicity, but also that it does so at a lower dose than cephalothin. These findings may in part explain the divergent observations regarding the nephrotoxicity of cephalothin-gentamicin combination therapy in rats and humans.
Animals↗
Comparative nephrotoxicity of SCH 21420 and amikacin in rats.
The nephrotoxic potentials of the new aminoglycoside SCH 21420 and amikacin were compared in a rat model. Groups of rats received 100, 200, 300, or 600 mg of either drug per kg per day for 14 days. Enzymuria, urine osmolality, protein excretion, and blood urea nitrogen were monitored at periodic intervals, whereas creatinine clearance and pathological changes were determined at sacrifice. Amikacin caused more enzymuria at the two lower doses as well as greater proteinuria and blood urea nitrogen elevations at the highest dose than did SCH 21420 (P less than 0.05). Pathological changes were more severe with amikacin than with SCH 21420 at the three lower doses (P less than 0.05); however, at the 600 mg/kg per day dose, the pathological scores and creatinine clearances of animals receiving either drug were not significantly different (P greater than 0.05).
Amikacin↗
Ferritin- and apoferritin-induced immune complex glomerulonephritis in mice.
In order to study the effects of the protein moiety independent of the protein-iron complex in the development of ferritin-induced glomerulonephritis, we compared the effects of ferritin, equimolar amounts of apoferritin, and equimolar amounts of iron dextran in Swiss albino mice. The results were compared to both saline-injected and non-injected controls. Ferritin resulted in a glomerulonephritis associated with predominantly mesangial deposition of immune complexes. Tubulo-interstitial changes occurred as well. Iron dextran resulted in similar but less severe tubulo-interstitial changes and evoked no glomerular alterations. Apoferritin resulted in an immune complex glomerulonephritis usually associated with membranous deposits. No tubular or interstitial changes occurred. Proteinuria developed in animals receiving apoferritin. Since the protein-iron complex caused tubular and interstitial damage, apoferritin may provide a more suitable model of immune-complex-mediated glomerulonephritis.
Animals↗
Long term effect of cis-diamminedichloride platinum (CDDP) on renal function and structure in man.
To examine CDDP induced nephrotoxicity in patients with testicular carcinoma, we measured renal function prior to therapy and at six month intervals for twelve months in fifteen patients and twenty-four months in seven patients. CDDP was given iv at 20 mg/M2 per day for five days at three week intervals. Eight patients received three courses, four received four courses and three received more than four courses. The mean creatinine clearance +/- SD prior to treatment was 112 +/- 12 ml/min. By six months, it had decreased to 68.5 +/- ml/min (p less than 0.01) and it remained at that level. Plasma creatinine and blood urea nitrogen increased significantly. Subjects receiving other potential nephrotoxins in addition to CDDP developed a greater decrease in creatinine clearance (p less than 0.05). Proteinuria and functional tubular disturbances were not observed. Microscopic features were characterized by hydropic degeneration of the renal tubular epithelium, thickened tubular basement membranes and mild interstitial fibrosis. Electron microscopy revealed phagolysosomes filled with flocculent material. CDDP resulted in a permanant, nonspecific renal injury in our patients. Although the renal injury has remained subclinical, future courses of CDDP may lead to clinically important chronic renal failure.
Adolescent↗
Asymptomatic IgA nephropathy associated with pulmonary hemosiderosis.
A glomerular lesion identical to that of IgA nephropathy was demonstrated unexpectedly in a 17 year old boy who presented with clinical manifestations of pulmonary hemosiderosis and with no evidence of renal disease. This subclinical glomerular lesion would have remained undetected in this patient unless kidney tissue was obtained and examined by immunofluorescence or electron microscopy. It is unknown if the glomerular lesion in this case is causally related to pulmonary hemosiderosis.
Adolescent↗
Comparative nephrotoxicity of aminoglycoside antibiotics in rats.
Netilmicin, gentamicin, tobramycin, amikacin, kanamycin, streptomycin, and sisomicin were given daily for 15 days to groups of rats at three dosage levels corresponding to 10, 15, or 25 times the dose recommended for humans on a weight basis. Decreased urinary osmolality and increased urinary excretion of protein and beta-N-acetyl hexosaminidase were dose-related features of nephrotoxicity. Decreased tubular resorption of glucose and phosphate were observed with the most toxic regimens after extensive renal damage had occurred. All aminoglycosides accumulated in renal tissue; however, the concentration of drug in the renal cortex at the time the rats were killed was not useful for the prediction of renal impairment. Streptomycin and netilmicin exhibited a flat dose-reponse curve with respect to histological damage, as compared with the curves for the other drugs. Results of studies of creatinine clearance and examination of renal tissue suggested the following order of increasing toxicity of the treatment regimens: (1) 0.9% NaCl and uninjected controls; (2) streptomycin; (3) netilmicin; (4) tobramycin; (5) sisomicin, amikacin, and kanamycin; and (6) gentamicin.
Amikacin↗
Nephrotoxicity of netilmicin in combination with non-aminoglycoside antibiotics.
To assess the possibility that non-aminoglycoside antibiotics may adversely affect the nephrotoxicity of the new semisynthetic aminoglycoside netilmicin, we gave ampicillin, carbenicillin, methicillin, cefamandole, and clindamycin, either singly or in combination with netilmicin, at two dose concentrations in rats. Results were compared as to the effect of netilmicin given singly and to saline-injected and noninjected controls. Antibiotic combinations resulted in no greater nephrotoxicity than did netilmicin alone. Netilmicin concentrations in renal tissue were high, and these levels were not consistently affected by the other drugs. The data suggest that in rats the nephrotoxicity of netilmicin is not affected adversely by the presence of non-aminoglycoside antibiotics.
Aminoglycosides↗
Recovery from aminoglycoside nephrotoxicity with continued drug administration.
To examine the nephrotoxicity of prolonged gentamicin administration compared to the effect obtained when a less toxic aminoglycoside is substituted during the course of treatment, we gave gentamicin (67.5 mg/kg per day) to rats for 21 days, gentamicin for 14 days followed by either netilmicin or tobramycin for 7 days, or gentamicin for 14 days followed by saline diluent. After initial tubular, necrosis, the animals recovered from renal injury whether the drug was continued or discontinued or another drug was substituted. These data are consistent with the observation that regenerating renal epithelium is resistant to continued or additional nephrotoxic insults. These findings suggest that improvement in renal function during aminoglycoside therapy cannot necessarily be attributed to the substitution of another aminoglycoside or other therapeutic interventions.
Animals↗
Effects of chronic tubular obstruction in Necturus kidney.
The effects of chronic single nephron or mesonephric duct obstruction on renal pressures were measured in anesthetized Necturi by servo-null techniques. Glomerular capillary hydrostatic pressure (PGC) averaged 11.3 +/- 1.2 (SD) cmH2O in 18 normal nephrons. Chronic tubule blockade for 2-6 days produced no significant change in PGC. Light and electron microscopy of the juxtaglomerular apparatus (JGA) revealed juxtaglomerular cell granules widely dispersed along the course of preglomerular arterioles, a deficient macula densa, and no polkissen. The absence of a detectable change in PGC with chronic tubule blockade, i.e., a tubuloglomerular feedback response, may reflect poor development of the JGA in this amphibian.
Animals↗
Rapidly progressive glomerulonephritis in adults: clinical and histologic correlations.
The clinical and histological features of 43 patients with rapidly progressive glomerulonephritis were reviewed. All had extensive crescent formation in more than 50 per cent of glomeruli. Three distinct patterns of immunofluorescent staining were identified: linear, granular, and sparse staining. Electron microscopy was valuable in corroborating the results of immunofluorescence. The prognosis was poor, with no patient regaining normal renal function regardless of treatment. Significant differences were observed among patients categorized by immunofluorescent staining. Those with a linear pattern were younger and more commonly had hemoptysis. Patients with sparse immunofluorescent staining had better renal function at the time of presentation and a longer duration of illness.
Adolescent↗
Gentamicin gradient patterns and morphological changes in human kidneys.
The gentamicin gradient pattern was studied in ten autopsied patients who expired during gentamicin therapy. Although two of the patients had acute renal failure, none was thought to have gentamicin-related nephrotoxicity. Gentamicin concentrations in cortex significantly exceeded those in medulla or serum (p less than 0.05 and p less than 0.01, respectively). No correlation was found between the cortical concentrations and the total drug dose, the time interval between the last injection and death, or the plasma creatinine concentrations in this heterogeneous group of patients. In addition, two specimens were suitable for electron microscopy which displayed cytosegrosomes and myeloid bodies previously noted in experimental animals. We conclude that gentamicin forms a gradient pattern in human kidney similar to that described in experimental animals. Furthermore, it evokes similar morphological changes.
Adolescent↗
The effect of concomitant mercuric chloride and gentamicin on kidney function and structure in the rat.
In order to define the possible effects of gentamicin on the course of experimental acute renal failure, the interaction between gentamicin and mercuric chloride was studied in rats. Acute renal failure was induced with 1 mg. of HgCl2 per kilogram intravenously. When given alone, HgCl2 produced a uniform, reproducible, nonoliguric, acute renal failure with a low mortality rate. Animals receiving gentamicin over the course of HgCl2-induced acute renal failure, in doses sufficient to produce a 1 hour postinjection serum concentration of 10 mug/ml., recovered glomerular filtration in a fashion similar to animals receiving only HgCl2(p greater than 0.05). Animals that recovered from HgCl2-induced acute renal failure were given 10 mg./Kg. of gentamicin every 4 hours for 15 days and developed proteinuria and decline in urine osmolality to the same degree as animals given gentamicin alone, but failed to develop azotemia. Nevertheless, morphological changes associated with gentamicin nephrotoxicity were found which were similar in severity to those seen with gentamicin alone. Animals pretreated with 10 mg./Kg. of gentamicin every 4 hours for 7 days were then given HgCl2. Acute renal failure in these animals was more severe than in animals receiving HgCl2 alone, as manifest by a greater degree of azotemia and death (p less than 0.05). The data indicate that in the rat the concomitant administration of gentamicin did not interfere with recovery from HgCl2-induced renal failure. Rats recovering from HgCl2-induced acute renal failure were resistant to a depression in glomerular filtration when given gentamicin. The prior administration of gentamicin enhanced the nephrotoxicity of HgCl2.
Acute Kidney Injury↗
Renal tubular injury in rats induced by sodium pentafluorostannite, a new anticariogenic agent.
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Animals↗