Cases reported "Diabetic Nephropathies"

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1/44. cyclosporine disposition and long-term renal function in a 500-pound kidney transplant recipient.

    Patient size has been suggested as a risk factor in kidney transplantation. We have followed a recipient of a cadaver kidney who became massively obese (232 kg, 511 lbs) 5 years posttransplantation. He has maintained stable renal function with no rejection episodes and at 5 years has a measured serum creatinine of 2.2 mg/dL, creatinine clearance 42 mL/min, and urinary protein excretion of 320 mg/24h. Both oral and intravenous cyclosporine (Sandimmune) pharmacokinetic studies were done on a steady-state dose of 150 mg, which represents 0.65 mg/kg per dose. The patient exhibited very high bioavailability, F = 95%, and an oral elimination T1/2 of over 21 hours. These data confirm that stable cyclosporine delivery in very obese recipients can be sustained by dosing normalized to the ideal body weight and trough level monitoring.
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2/44. Effect of camostat mesilate on urinary protein excretion in three patients with advanced diabetic nephropathy.

    Effective treatment has not yet been established for patients with persistent proteinuria and hypoproteinemia related to advanced diabetic nephropathy. We report three patients with diabetic nephropathy presented with the nephrotic syndrome who showed a marked decrease in proteinuria following the administration of camostat mesilate, a protease inhibitor. Each patient was resistant to treatment with an angiotensin-converting enzyme (ACE) inhibitor and a platelet-aggregation inhibitor. Camostat mesilate, 600 mg/day, orally, caused a marked decrease in urinary protein excretion after the 7th consecutive day of drug administration. There were no serious adverse effects. Its mechanism of action in this respect is not known. Camostat mesilate thus merits clinical trials in the treatment of nephrotic syndrome related to diabetic nephropathy.
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3/44. Emphysematous pyelonephritis: case report and review of the literature.

    Emphysematous pyelonephritis (EP), a rare necrotizing infection of the upper urinary tract, is a life-threatening complication of patients with diabetes mellitus. A case of EP is described where the diagnosis was delayed for 36 h and the patient died notwithstanding aggressive medical and surgical intervention. The demonstration of gas in the renal structures is pathognomonic of EP. Because early diagnosis and aggressive medical and surgical management is imperative for recovery, we recommend plain abdominal radiographs as a minimal screening tool for all diabetic patients who present to hospital with a presumptive pyelonephritis. The diagnosis should also be considered in patients who failed appropriate medical therapy.
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4/44. mycobacterium avium complex pleuritis accompanied by diabetes mellitus.

    A 72-year-old woman with diabetic nephropathy was hospitalized with peripheral edema in the extremities and weight increase. After diuretics and human serum albumin administration, her condition improved. From the 15th day she had run a subfever and her breathing was diminished in the left lower lung field. A plain chest x-ray film showed pleural effusion over the left lung field. The fluid was exudative. Fluid cultures were negative. A tuberculin reaction was negative. polymerase chain reaction method disclosed mycobacterium avium complex, indicating rare pleuritis due to mycobacterium avium complex. Eighteen days after chemotherapy, pleural effusion disappeared. Although her hemoglobin A1c (HbA1c) levels were maintained from 6.0 to 6.5% over 4 years, urinary albumin excretion levels and serum creatinine levels increased, indicating deteriorating diabetic nephropathy. serum albumin levels remained low (3.3-3.6 g/dl). malnutrition, impaired cellular immunity and apparently abnormal microvascular circulation due to diabetes mellitus may consequently have induced pleuritis due to mycobacterium avium complex.
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5/44. Fatal emphysematous pyelonephritis with gas in the spinal extradural space in a patient with diabetes.

    BACKGROUND: Emphysematous pyelonephritis (EP) is a rare but life-threatening condition of the upper urinary tract, characterized by the presence of gas in the renal parenchyma and perirenal space. The vast majority of patients with EP (90%) are known to have diabetes, with escherichia coli being the most common causative pathogen. CASE REPORT: We present a case of fatal bilateral EP in a patient with diabetes, with an unusual radiological finding of gas around the spinal cord and in the psoas muscle, with renal parenchymal sparing. Our case serves as an important reminder of this life threatening entity in diabetic patients, which is not well recognized by clinicians because of its rarity.
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6/44. Reversible acute renal failure and nephrotic syndrome in a Type 1 diabetic patient.

    nephrotic syndrome is a condition commonly associated with end-stage renal disease secondary to diabetic nephropathy. It is usually associated with long-standing renal insufficiency, microalbuminuria, and overt proteinuria. We present a diabetic patient with acute oliguric renal failure and nephrotic syndrome. At presentation, he had a serum creatinine of 2.3 mg/dl, blood urea nitrogen (BUN) of 69 mg/dl, urinary protein excretion of 10.5 g/24 h, serum albumin of 1.3 g/dl, and a urine output < 400 cc/24 h. A renal biopsy was done and the renal pathology was compatible with early diabetic nephropathy. Despite intense diuretic therapy, the patient's renal condition did not improve, and peritoneal dialysis was started several months after diagnosis. After 8 months of dialysis therapy, the patient's renal parameters and urinary output spontaneously restored to normal limits (serum creatinine was 1.1 mg/dl, urinary albumin excretion was 411 mg/24 h, serum albumin was 4.3 g/dl, and normal urine output) and dialysis was discontinued. His renal function did not deteriorate after discontinuation of dialysis. We conclude that this patient's reversible acute renal failure and nephrotic syndrome were associated with minimal change disease and not due to diabetic nephropathy.
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7/44. Nephrogenic diabetes insipidus due to demethylchlortetracycline hydrochloride in a child.

    Nephrogenic diabetes insipidus occurred in a 7-year-old child who had received a high dose of demethylchlortetracycline hydrochloride (DMC). The patient had a relatively elevated urinary sodium concentration in addition to isosthenuria. The nephrogenic diabetes insipidus was completely reversible within one month after cessation of DMC administration.
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8/44. Exacerbation of the ochronosis of alkaptonuria due to renal insufficiency and improvement after renal transplantation.

    In alkaptonuria, homogentisate 1,2-dioxygenase deficiency causes tissue accumulation of homogentisic acid (HGA), followed by signs and symptoms of ochronosis. These include massive urinary excretion of HGA, arthritis and joint destruction, pigmentation of cartilage and connective tissue, and cardiac valve deterioration. We describe a 46-year-old man with alkaptonuria and diabetic renal failure whose plasma HGA concentration was twice that of any other alkaptonuria patient, and whose ochronosis progressed much more rapidly than that of his two alkaptonuric siblings. After renal transplantation, the plasma HGA normalized, and the daily urinary excretion of HGA decreased by 2-3g. This case illustrates the critical role of renal tubular secretion in eliminating HGA from the body, and suggests that renal transplantation in a uremic patient not only restores HGA excretion, but may also provide homogentisate 1,2-dioxygenase activity for the metabolism of HGA.
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9/44. Possible participation of a prostaglandin E1 analogue in the aggravation of diabetic nephropathy.

    A relation between the progression of diabetic nephropathy and glomerular hyperfiltration has been speculated. We describe two cases of non-insulin-dependent diabetic males aged 55 and 59 years in whom diabetic nephropathy was aggravated during the administration of limaprost, a a prostaglandin E1 analogue with a vasodilatory action. We also observed a short-term effect of limaprost on renal hemodynamics in three cases with diabetic nephropathy. In case 1, one year after limaprost administration the serum albumin level fell from 3.6 to 2.6 g/dl and the serum creatinine level rose from 1.0 to 1.6 mg/dl. In case 2, 9 months after limaprost administration the serum albumin level fell from 3.6 to 2.9 g/dl and the serum creatinine level rose from 1.8 to 2.3 mg/dl. In the latter stages of limaprost administration, the downslopes of reciprocal serum creatinine against time appeared to be augmented in the two cases. After the 3-day administration of limaprost, the peripheral and renal blood flows, and the glomerular filtration rate (GFR) were observed to rise, but the filtration fraction (FF) and urinary protein output were elevated. Keeping in mind the pre-existing renal damage, the increases in GFR and FF suggested acceleration of compensatory glomerular hyperfiltration in less damaged surviving glomeruli. The sustained acceleration of hyperfiltration with long-term administration of limaprost as an exogenous vasodilatory prostaglandin was assumed to eventuate in the aggravation of diabetic nephropathy. attention should be paid to drugs which increase GFR in patients with established diabetic nephropathy.
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10/44. Highly resistant metabolically deficient dwarf mutant of escherichia coli is the cause of a chronic urinary tract infection.

    We present the case of a 68-year-old diabetic woman who has been suffering from chronic urinary tract infections, recurring over a period of at least 5 years, caused by a slowly growing metabolically deficient dwarf mutant (MDD) of escherichia coli. This MDD strain was auxotrophic for histidine, was resistant to multiple antibiotics, and showed atypical growth behavior. Colonies were tiny on routine media but were able to revert to normal growth after extended incubation. This strain was identified as E. coli by 16S ribosomal dna sequencing, and virulence factor profiles were determined by PCR. Seven MDD isolates collected over the 5-year period were grown from midstream urine to significant colony counts and shown to belong to the same clonal group by pulsed-field gel electrophoresis and enterobacterial repetitive intergenic consensus PCR. These MDDs were repeatedly misidentified by biochemical methods due to their slow growth and atypical colony morphology. This case highlights the importance of recognizing MDDs of enterobacteriaceae in patients with chronic infections. To our knowledge this is the first report of an MDD of E. coli causing a chronic urinary tract infection.
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