Cases reported "Diabetes Mellitus, Type 2"

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21/33. Acute myopathy in a type 2 diabetic patient on combination therapy with metformin, fenofibrate and rosiglitazone.

    AIMS/HYPOTHESIS: This report describes the case of a 75-year-old male type 2 diabetic Caucasian who was admitted to the clinical ward because of acute pain and cramps in both calf muscles. MATERIALS AND methods: Neuromuscular function was assessed by electromyography and electroneurography of the right leg. An open biopsy was taken from the left vastus lateralis muscle for histological and histochemical analyses. Southern blotting was performed to detect defects in mitochondrial dna and tRNA. Cytochrome P450 (CYP-P450) polymorphisms were analysed in blood cells. RESULTS: Fifteen weeks before admission, the patient's lipid-lowering medication was switched from simvastatin to fenofibrate because of predominant hypertriglyceridaemia; this did not affect creatine kinase levels. Three weeks before admission, rosiglitazone was added to his existing metformin therapy because of worsening metabolic control. Upon admission, serum enzymes indicating myopathy were elevated (creatine kinase 6897 U/l, myoglobin 902 ng/ml) and kidney function was impaired (creatinine 0.116 mmol/l, blood urea nitrogen 2.3 mmol/l). electrophysiology revealed myopathy and sensory polyneuropathy. histology showed multiple damage of the myofibrillar architecture. There was no evidence of defects in mitochondrial dna or tRNA. Furthermore, no functional limitations in CYP2C9, CYP2C19 and CYP2D6 were detected. Following withdrawal of the oral medication and intravenous hydration, clinical symptoms and laboratory parameters gradually decreased. CONCLUSIONS/INTERPRETATION: Until more data from controlled trials are available, we recommend that combination therapy with fibrates and thiazolidinediones should be monitored frequently by measurements of serum creatine kinase and creatinine, specifically in patients with pre-existing nephropathy and polyneuropathy.
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22/33. Severe pancreas hypoplasia and multicystic renal dysplasia in two human fetuses carrying novel HNF1beta/MODY5 mutations.

    Heterozygous mutations in the HNF1beta/vHNF1/TCF2 gene cause maturity-onset diabetes of the young (MODY5), associated with severe renal disease and abnormal genital tract. Here, we characterize two fetuses, a 27-week male and a 31.5-week female, carrying novel mutations in exons 2 and 7 of HNF1beta, respectively. Although these mutations were predicted to have different functional consequences, both fetuses displayed highly similar phenotypes. They presented one of the most severe phenotypes described in HNF1beta carriers: bilateral enlarged polycystic kidneys, severe pancreas hypoplasia and abnormal genital tract. Consistent with this, we detected high levels of HNF1beta transcripts in 8-week human embryos in the mesonephros and metanephric kidney and in the epithelium of pancreas. Renal histology and immunohistochemistry analyses of mutant fetuses revealed cysts derived from all nephron segments with multilayered epithelia and dysplastic regions, accompanied by a marked increase in the expression of beta-catenin and E-cadherin. A significant proportion of cysts still expressed the cystic renal disease proteins, polycystin-1, polycystin-2, fibrocystin and uromodulin, implying that cyst formation may result from a deregulation of cell-cell adhesion and/or the Wnt/beta-catenin signaling pathway. Both fetuses exhibited a severe pancreatic hypoplasia with underdeveloped and disorganized acini, together with an absence of ventral pancreatic-derived tissue. beta-catenin and E-cadherin were strongly downregulated in the exocrine and endocrine compartments, and the islets lacked the transporter essential for glucose-sensing GLUT2, indicating a beta-cell maturation defect. This study provides evidence of differential gene-dosage requirements for HNF1beta in normal human kidney and pancreas differentiation and increases our understanding of the etiology of MODY5 disorder.
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23/33. Renal failure due to cholesterol embolization following percutaneous transluminal renal angioplasty.

    Percutaneous transluminal renal angioplasty was performed in a 63-year-old diabetic woman who had renovascular hypertension with solitary functioning kidney and diffuse atherosclerosis. angioplasty was technically successful, while thereafter, fever and myalgia of legs occurred with gradual increases in blood urea nitrogen and creatinine. The patient became uremic over a month after angioplasty and was placed on dialysis. She died six months after angioplasty. autopsy revealed cholesterol embolization in bilateral kidney, pancreas and spleen, causing subacute renal failure. It is suggested that careful assessment of the patient should be made when determining the need for renal angioplasty for renovascular hypertension with a solitary functioning kidney.
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24/33. Effect of unilateral nephrectomy on three patients with histopathological evidence of diabetic glomerulosclerosis in the resected kidney.

    diabetes mellitus and surgical ablation of renal tissue are two independent influences associated with hyperfiltration and elevated levels of the glomerular transcapillary hydraulic pressure differential (delta P). There is increasing evidence that hyperfiltration with elevated delta P is pathogenic and leads to glomerular damage. The authors questioned whether these two influences (surgical ablation of renal tissue and diabetes mellitus) would act in an additive fashion in human patients to produce an accelerated decline in renal function. Three patients with non-insulin-dependent diabetes mellitus who had undergone a unilateral nephrectomy (for a variety of reasons) were (retrospectively) identified. In each patient, morphologic evidence of diabetic glomerulonephropathy was present in the resected kidney. The charts from these patients were reviewed and post-nephrectomy renal function was estimated over time by plotting reciprocal serum creatine values versus time. Follow-up intervals after nephrectomy varied from 4 to 15 years. The results of our follow-up showed no obvious detrimental effect on renal function (as measured by 1/serum creatinine) attributable to the unilateral nephrectomy. The authors conclude that residual renal function (and ultimate outcome) in patients with non-insulin-dependent diabetes mellitus is highly variable, but does not seem to be adversely affected (at least over the time span of observation in these patients) by unilateral nephrectomy.
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25/33. nephrotic syndrome associated with angiofollicular lymph node hyperplasia.

    A women presented at the age of 22 with anemia, hepatosplenomegaly, polyclonal hypergammaglobulinemia and a mediastinal shadow. At thoracotomy she had enlarged mediastinal lymph nodes which displayed histological features typical of angiofollicular hyperplasia. Marrow plasmacytosis was present. She developed diabetes mellitus at the age of 29 yrs after she had received oral steroid treatment for one year. The nephrotic syndrome supervened another year later. Her kidneys were enlarged before the onset of diabetes. The glomerular changes included a marked increase of mesangial matrix and segmental hypercellularity. The association of the nephrotic syndrome and angiofollicular lymph node hyperplasia is extremely rare and their interrelation remains enigmatic.
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26/33. Unilateral nodular diabetic glomerulosclerosis: recurrence of an experiment of nature.

    The case of a 60-year-old diabetic patient with a fully developed diabetic glomerulosclerosis in one kidney, but only ischemic lesions in the contralateral one, which was 'protected' by a renal artery stenosis, is presented. The only other report of such a peculiar observation was made by Berkman and Rifkin on a patient who died in 1940. Because of the rather high incidence of diabetes and of renal artery stenosis, the scarcity of this 'experiment of nature' is astonishing and can be barely explained by a precise timing of the two pathological conditions. Despite rather detailed information on the clinical and paraclinical evolution of the present patient, the exact sequence of events could not be determined with certitude. Both cases bring a strong support for the role of glomerular hyperperfusion-hypertension in the pathogenesis and evolution of diabetic nephropathy and provide a theoretical basis for the importance of keeping the arterial pressure low in diabetics.
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27/33. Diabetic renal hypouricemia.

    In diabetes, the serum uric acid level is low due to increased urate clearance; however, its mechanism remains unknown. We examined seven maturity-onset diabetic patients with rarely reported hypouricemia due to renal tubular abnormality to better understand the renal handling of urate by the diabetic kidney. The results of studies indicate that the increase in urate clearance was entirely accounted for by increased pyrazinamide-suppressible urate clearance. The maximal uricosuric response to probenecid administration was exaggerated. The effects of drugs on urate clearance were similar to those we have previously reported in the syndrome of inappropriate secretion of antidiuretic hormone. In four patients, the family survey did not reveal anyone with hypouricemia. These observations suggest that hypouricemia due to hyperuricosuria, which responds markedly to pyrazinamide and probenecid, is actually an indicator of renal tubular abnormality in diabetics.
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28/33. fibromuscular dysplasia: an unusual cause of hypertension in the transplant recipient.

    A transplant recipient developed hypertension from unsuspected fibromuscular dysplasia of the donor renal artery. We believe this is the first reported case of this disease transmitted by transplantation. Successful repair of the stenosis was obtained by resection of the stenotic area and reanastomosis to the internal iliac artery. While the diagnosis of fibromuscular hyperplasia was not suspected in our donor prior to organ retrieval, its eventual occurrence in the transplanted kidney suggests that when the donor clinical picture is appropriate the lesion should be searched for prior to use of the organs.
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29/33. Acute graft loss secondary to necrotizing vasculitis. Evidence for cytokine-mediated Shwartzman reaction in clinical kidney transplantation.

    A small number of kidney transplant recipients abruptly lose function secondary to acute renal artery or vein thrombosis or more rarely a form of necrotizing vasculitis. We report a group of four kidney transplant recipients who lost renal function and share the following features: (1) diabetes (type I, insulin-dependent diabetes mellitus, type II or steroid-induced); (2) abrupt change/loss of renal function; (3) a concomitant clinical event (fever, viral symptoms, menometrorrhagia, viremia, bacteremia); (4) severe necrotizing vasculitis with hemorrhagic necrosis on histopathology; (5) patent renal artery and vein at time of transplant nephrectomy (i.e., no vascular thrombosis); and (6) high levels of peripheral serum gamma-IFN 1-5 days before transplant nephrectomy (467 /- 175 pg/ml) compared with that of patients experiencing severe rejection (8.4 /- 3.7 pg/ml) (P < 0.002). These data support the concept of a cytokine (IFN-gamma)-mediated accelerated inflammatory response resulting in graft loss from necrotizing vasculitis--the clinical equivalent of an organ-specific Shwartzman reaction.
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30/33. adult-onset diabetes mellitus and neurosensory hearing loss in maternal relatives of MELAS patients in a family with the tRNA(Leu(UUR)) mutation.

    We describe a family with three cases of "clinically incomplete mitochondrial encephalomyopathy, lactic acidosis, and strokelike episodes (MELAS) syndrome" in which heteroplasmic tRNA(Leu(UUR)) mutation at nucleotide 3243 of the mitochondrial dna was present in three generations. The amount of mutant genome varied among tissues: it was 60% in the kidney, 72% in the cardiac muscle, and 91% in the liver of the female proband's affected brother and 63% in the kidney, 71% in the cardiac muscle, and 71% in the liver of the female proband's perinatally deceased son. The tRNA(Leu(UUR)) mutation was also carried by the siblings of the proband's affected mother. None of them had any clinical signs of melas syndrome. This syndrome has the new feature of being associated with adult-onset diabetes mellitus, neurosensory hearing loss, and short stature.
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