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At least 19 recordsLinked to original sources

Experimental studies on hematogenously induced renal damage in the rabbit due to Pseudomonas aeruginosa.

Chronic systemic infections of rabbits were established by intravenous inoculation of 4 times 10-8 P. aeruginosa cells in order to study the sequence of events leading to severe kidney damage. Renal lesions were detected by the fifth- to seventh-day postinfection, as were lesions in the liver and lungs. Progressive azotemia led to death by the 12th-16th day. Lesions in the kidneys, lungs and liver were characterized terminally by intense mononuclear cell infiltrates, hemorrhage, and microabscess formation. Mononuclear cells also appeared to be the predominant responsive cell early in infection. There appeared to be no difference in the susceptibility to infection or severity of renal lesions between rabbits with surgically induced unilateral ureteral obstruction and nonobstructed rabbits.

Animals

[Acute hepatic failure and renal damage. Experimental and clinical studies].

Renal damage in acute hepatic failure induced in the pig by means of an hepatic state, temporary or permanent devascularisation Amanita phalloides poisoning or orthotopic liver transplant proved of slight degree, particularly in animals treated with replacement therapy. In the cases of animals that died in acute hepatic coma, on the other hand, renal cortex ischaemia and marked medullary congestion were constant. Histologically, the damage consisted of slight tubular nephrosis; this was more apparent in the proximal tubules. Evaluation of renal damage in 38 patients with acute hepatic failure was more complicated owing to the variety of clinical conditions (level of coma, hypovolaemia, intensive care and hepatic assistance). Nevertheless, a clear relation was established between the degree of liver damage and blood creatinine and creatinine clearance values. All patients who died presented liver cell necrosis of over 75%, blood creatinine values of more than 2 mg/100 ml, and less than 50 ml/min clearance. Tubular nephrosis was the predominant lesion. It appeared that renal damage was primarily pre-renal. No signs of a true hepatorenal syndrome could be made out.

Animals

An experimental model of analgesic-induced renal damage--some effects of p-aminophenol on rat kidney mitochondria.

1. p-Aminophenol, a known nephrotoxin, has been studied as a model for phenacetin-induced renal damage. 2. Respiration, oxidative phosphorylation and ATPase activity were inhibited in mitochondria isolated from the kidneys of treated rats; this could not be reversed by the addition of exogenous loosely bound cofactors and bovine serum albumin to the assay medium. 3. After treatment the mitochondrial levels of sodium and calcium were increased, potassium decreased and magnesium unaltered. 4. Mitochondria isolated from treated rats showed ultrastructural damage. 5. The results are interpreted to indicate that renal tubular cell mitochondrial injury is important in triggering cortical analgesic renal damage.

Adenosine Triphosphatases

Renal damage with intestinal bypass.

Renal function and biopsies were studied in 18 patients, 7 to 108 months after intestinal bypass. Enteropathy was found in 12 and hyperoxaluria in 16. Every biopsy showed a type of focal interstitial nephritis, tubular atrophy, fibrosis, and glomerular hyalinization. Damage ranged from minimal to extensive and renal function from normal to end-stage failure. Tubular injury had resulted partly from oxalate deposits. However, in 10 patients no oxalate crystals were seen. In eight others, most of the damaged areas were remote from crystal deposits. Immunoglobulin M and C3 deposits, found in glomerular capillaries and the messangium in six of 11 specimens, and the presence of circulating immune complexes in five of 10 patients, in addition to the extraintestinal organ involvement, suggested immune complex mesangial injury as one factor in bypass nephropathy. With progressive impairment of renal function, a biopsy appears justified. If damage is significant, the bypass should be dismantled.

Adult

Occult progressive renal damage in the elderly male due to benign prostatic hypertrophy.

A review of the case histories of 345 patients who underwent protatectomy showed that 1.7 percent (6 patients) had "occult and progessive renal damage" secondary to prostatic hypertrophy. All these men were over the age of 60 and the disturbances in micturition were so mild that the patients were unaware of, or chose to ignore them. The presenting symptoms were nonspecific and included generalized weakness, anorexia, nausea, constipation, and weight loss. Investigation revealed impaired renal function of varying degrees. Prostatectomy was associated with a dramatic improvement in all 6 patients. Physicians should be aware of the clinical entity of occult and progressive renal damage secondary to obstruction of the bladder outlet, especially in the elderly male. Uremia can develop with minimal urinary symptoms. Elderly men often suppress or deny their symptoms because of the fear of operation.

Age Factors

Recessive X-linked hyperuricemia with gout and renal damage, normal activity of hypoxanthine phosphoribosyltransferase and resistance to azaguanine.

A family is reported where four males have developed hyperuricemia, renal damage and, except for the youngest person affected, gout at an early age. The disease appears to be inherited as an X-linked recessive metabolic error. Clinically the patients have developed classical, tophaceous gout before the age of 25 and have suffered repeated attacks of renal colic. Renal tubular damage with decreased ability to concentrate and acidify urine was seen in a family member of only 16 years of age. Progressive renal failure seems to develop slowly. None in the family has shown neurologic symptoms, and two of the four affected men are apparently of at least average intelligence, two slightly below average. One female carrier has repeatedly passed uric acid stones. Studies of the red blood cell lysate have shown a normal activity of enzyme hypoxanthine phosphoribosyltransferase, and an increased level of adenine phosphoribosyltransferase. Skin fibroblasts from affected family members grew normally in the presence of 8-azaguanine. Administration of azathioprine to the patients did not decrease their serum uric acid levels. This is the first family described with this type of disorder of the purine metabolism.

Adenine Phosphoribosyltransferase

Renal damage in systemic lupus erythematosus with normal renal function.

Renal biopsies were performed on 12 patients with definite systemic lupus erythematosus (SLE) with normal renal function. Three had had previous nephropathy which responded to treatment, with return of urinalysis and function to normal. Specimens were studied using light microscopy (LM), immunofluorescence (IF), and electron microscopy (EM). Mild to moderate abnormalities were found in all patients. Changes by LM (primarily hypercellularity) were found in 11 specimens (no glomeruli were obtained in one) and classified as inactive. IF studies were positive in eight of the 12 biopsies with either focal or diffuse distribution of IgG, IgM, and/or C3. EM changes were observed in all cases and were of mild to moderate severity. They included focal to multifocal glomerular hypercellularity, basement membrane thickening, foot process fusion, and mesangial and intramembranous electron dense deposits. No subepithelial or subendothelial deposits were found. Microtubular structures were present in three specimens. These data suggest that careful study of renal biopsy specimens may reveal evidence of kidney involvement in all patients with SLE.

Antibodies, Antinuclear

Renal damage associated with long term use of lithium carbonate.

The authors report 2 cases of renal damage associated with lithium carbonate treatment. The relevant literature is reviewed and supports the claim that the lithium ion may be nephrotoxic. The article concludes with practical recommendations for clinical practice until futher evidence regarding this association is available.

Adult

Sex differences in renal damage induced in the mouse by Amanita virosa.

The sensitivity of male and female mice to Amanita virosa was compared. Dried, homogenized mushroom was given orally by stomach tubing at doses of 100, 200, 400 and 800 mg dried mushroom/kg body weight. Both in males and in females, the kidneys were the only organs showing macroscopical changes. The dose of 100 mg/kg caused renal damage in females, whereas in males the first signs of kidney damage were seen at the dose of 400 mg/kg. The renal lesions observed in the males were located in the cortex, while in the females they were limited to the outer stripe of the outer medullary zone. Testectomy diminished the nephrotoxicity of A. virosa in male mice and caused changes in the localization of renal lesions.

Amanita

Induction of extraglomerular renal damage in experimental chronic serum sickness. I. Histologic and immunofluorescence findings.

Histologic and immunofluorescence studies were performed in nine rabbits after daily administration of human serum albumin at a fixed dosage for periods up to 26 weeks. All but one of the rabbits studied by immunofluorescence showed IgG, C3, and fibrinogen deposits in the renal glomeruli and in the tubules or peritubular tissues. In most cases, human serum albumin could also be identified in the deposits. In two rabbits killed at week 10, kidney pathology was minimal; in one of the rabbits killed in the early phases of the disease and in all rabbits killed after week 20, there were obvious pathologic changes affecting glomeruli, tubules, and/or interstitium. Tubulointerstitial changes were absent in only one of the rabbits killed at late stages of human serum albumin administration, in spite of evidence of tubular deposition of immune complexes. These observations suggest that tubulointerstitial damage is at least as frequent as glomerular damage during the induction of chronic serum sickness.

Animals

Tapered ileum as ureter substitute in severe renal damage: antireflux technique for bladder implantation.

Three cases are reported in which ileum has been used to replace irreparably damaged ureters despite preexisting moderate to severe pyelocaliectasis. Two cases have had satisfactory results while one had increasing pyelocaliectasis and azotemia requiring subsequent cutaneous diversion. The rationale for using ileum to replace ureter is presented with a discussion of objectives to be achieved surgically to assure the success of the procedure.

Adolescent