Biopsy renal

Kidney Fever, graft tenderness and swelling, decreased urine output, malaise, hypertension, weight gain, edema Increased SCr, BUN, leukocytosis, renal biopsy positive for lymphocytic infiltration... 

Histopathological evidence of renal damage has been observed in lead-exposed workers. Renal ultrastructure and function were examined in five men with heavy occupational exposure to lead (Cramer et al. 1974). In addition, renal function was evaluated in two men from whom renal biopsies were not obtained. PbB levels ranged from 71 to 138 pg/dL. Renal function tests were normal in all except for a reduced glomerular filtration rate in one worker. Two subjects with relatively short exposure to lead (6 weeks and 8 months) and PbB levels of 89-129 pg/dL had intranuclear inclusions in the proximal tubules. Renal biopsies from workers with longer periods of lead exposure (4-20 years, PbB levels of 71-138 pg/dL) had diffuse interstitial or peritubular fibrosis. Glomeruli were normal in all subjects. 

Renal Effects. Ingestion of drinking water containing lead was found to be associated with evidence of renal insufficiency in humans (Campbell et al. 1977). Lead concentrations in drinking water were compared to PbB concentrations in 283 residents who ingested this water for a mean of 21.5 years. A highly significant correlation was found for these two parameters. In addition, elevated PbB concentrations were associated with renal insufficiency, reflected as raised serum urea concentrations and hyperuricemia. No renal biopsies were performed. 

In some human studies where clinical chemistry measurements but no renal biopsies were performed, the only parameter of renal function shown to be affected was an increase in the levels of NAG in the urine. NAG is a lysosomal enzyme present in renal tubular cells that has been shown to be a sensitive indicator of early subclinical renal tubular disease. The mechanism by which lead affects the release of NAG from renal tubular cells is not known, but it is suggested that lead could attach to kidney cell membranes and alter membrane permeability (Chia et al. 1994). 

Nasr SH, Galgano SJ, Markowitz GS, et al. Immunofluorescence on pronase-digested paraffin sections a valuable salvage technique for renal biopsies. Kidney Int. 2006 70 2148-2151. 

This syndrome is characterized by proteinuria >3.5 g/day, hypoalbuminuria <3 g/dl, hyperlip-idaemia with an elevation of serum cholesterol, edema and oval fat bodies and fatty casts in the urinary sediment. A variety of disorders may produce nephrotic syndrome but, in the majority of cases, no cause is found. It is appropriate to define the selection of studies from the history and physical examination. Tests to order are antinuclear antibody, rheumatoid factor, cryoglobulins, serum complement, HBsAg VDRL serology (syphilis), protein electrophoresis of the serum and urine and HIV. If the cause is unclear a renal biopsy is done to define the glomerular lesion as treatment may on the underlying glomerular lesion. 

Single drug therapy is mostly adequate in lupus nephritis (LN) classified as renal biopsy WHO Class I and II. Single drug therapy in lupus nephritis Class III-V, and in particular Class VI is less or not effective. One immunosuppressant cannot suppress all aspects of autoimmune inflammation in the more serious forms of the disease. The SBC-5-IMNs is not required in Class I, IL and also not in Class VI. In Class VI nothing helps, except renal dialysis or renal transplantation. 

In a 23-year-old woman, a kidney allograft recipient with recurrent lymphoceles treated with povidone-iodine irrigations (50 ml of a 1% solution bd for 6 days), a metabolic acidosis occurred and renal function deteriorated. After a few days, despite suspension of irrigation, the patient developed oliguria, and dialysis was needed. A renal biopsy showed acute tubular necrosis. 

A 59-year-old woman with hemolytic-uremic syndrome and a recent history of atypical chest pain was given prophylactic desmopressin 0.4 micrograms/kg immediately before a renal biopsy (28). Within 30 minutes she developed chest pain and bradycardia due to myocardial infarction. 

The cytoplasmic part of nephrin interacts also with ZO-1 protein and actin (K10). Interaction of the antibody or toxin with the extracellular part of nephrin could thus also result in intracellular signaling (phophorylation of tyrosine residues in the cytoplasmic part of nephrin), change of the actin cytoskeleton, and foot process fusion. Indeed, increased levels of phosphotyrosine were demonstrated in renal biopsies of patients with minimal change disease and membranous nephropathy (B2). 

Wesson DE, Kurtzman NA, Prommer JP. Massive obesity and nephrotic proteinuria with a normal renal biopsy. Nephron. 1985 40 235-237. 

Chiu KY, Chin KW. Rapid immunofluorescence staining of human renal biopsy specimens using microwave irradiation. J. Clin. Pathol. 1987 40 689-692... 

Renal disease is detected through urinanaly-sis done yearly on PIZZ individuals with liver disease. Detection of proteinuria would lead to examination of a quantitative 24-hour urine for protein. If confirmation of the diagnosis is essential, then renal biopsy would be necessary. 

CM appears to have developed diabetic nephropathy, although a renal biopsy would be required to establish the definitive diagnosis. Approximately 40% of people with longstanding type 1 diabetes develop diabetic nephropathy. 

A 48-year-old man taking lithium and chlorprothixene had a creatinine clearance of 60 ml/minute and a renal biopsy showing chronic interstitial nephritis (380). 

Nephrotic syndrome (proteinuria, edema, hypoalbumine-mia, hyperlipidemia) is a rare and idiosyncratic complication of lithium therapy it usually resolves on withdrawal, and can recur on rechallenge (397,398). Lithium-associated nephrotic syndrome occurred in a 59-year-old woman with lithium toxicity (serum concentration 1.9 mmol/1) whose renal biopsy showed focal segmental glomerulosclerosis. Lithium withdrawal led to resolution of edema and marked improvement in proteinuria and albuminemia (398). 

In one subject, fever and spastic movements of Che head were noted he was treated vigorously with antidotes. At 3 h, he became unresponsive, showed decerebrate rigidity, had a high heart rate, and had urinary retention he was treated vigorously with antidotes. Five years later (1968), he was hospitalized for microscopic hematuria and was shown by renal biopsy to have focal glomerullcls. 

A 58-year-old Japanese woman with CREST syndrome (calcinosis, Raynaud s syndrome, esophageal sclerosis, sclerodactyly, and telangiectasia) developed progressive renal dysfunction (16). Renal biopsy showed changes typical of Chinese herb nephropathy. Analyses of Chinese herbs she had taken for several years demonstrated the presence of aristolochic acid. Oral prednisolone improved her renal function and anemia. 

A 59-year-old man developed renal insufficiency after self-medication for 5 years with a Chinese herbal remedy to treat his hepatitis (17). Renal biopsy showed signs characteristic of Chinese herb nephropathy. Analysis of the remedy proved the presence of aristolochic acids I and II. 

In Japan two cases of Chinese herb nephropathy were associated with chronic use of Aristolochia manchuriensis (Kan-mokutsu) (24). The diagnosis was confirmed by renal biopsy and the toxic constituents were identified as aristolochic acids I, II, and D. 

Taiwanese authors have reported 12 cases of suspected Chinese herb nephropathy, confirmed by renal biopsy (25). Renal function deteriorated rapidly in most patients, despite withdrawal of the Aristolochia. Seven patients underwent dialysis and the rest had slowly progressive renal insufficiency. One patient was subsequently found to have a bladder carcinoma. Other cases have been reported from mainland China (26) and Taiwan (27). 

A 31-year-old man developed a headache, nausea, and vomiting. He had taken ascorbic acid, 2-2.5 g/day and before the onset of symptoms up to 5 g/day. He had a raised serum creatinine (1000 qmol/l). Renal ultrasound showed increased cortical echogenicity, and a renal biopsy showed acute tubular necrosis and massive oxalate deposition. He was given pyridoxine and two sessions of hemodialysis. 

A 17-year-old girl took 25 tablets of bismuth subcitrate 300 mg (total 7.5 g) in a suicide attempt and developed severe renal insufficiency (34). Renal biopsy showed evidence of acute tubular necrosis, with epithelial flattening, lumen widening, and atrophic changes in the convoluted tubules and mononuclear cell infiltration and edema in the interstitium. She was managed with hemodialysis and recovered. 

Acute renal insufficiency with tubular necrosis has been described (14). It occurred within 24 hours of the first dose of captopril and required hemodialysis for 8 weeks. The diagnosis of ischemic tubular necrosis was confirmed by renal biopsy. Few previous cases of ACE inhibitor-induced nephropathy have been documented by renal biopsy. 

A 29-year-old man received a double lung transplantation for end-stage cystic fibrosis. After uneventful surgery, he was accidentally given ten times the intended dose of ciclosporin (30 instead of 3 mg/kg) and 18 hours later became anuric. His blood ciclosporin concentration was 4100 ng/ml. Hemodialysis was required for 6 weeks. A renal biopsy 7 weeks later showed typical features of acute tubular necrosis and lesions that resembled chronic nephrotoxicity. Renal function was stiU abnormal when he died from another cause 14 weeks after the accidental overdose. 

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