Cases reported "Diabetes Mellitus, Type 2"

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1/33. An unusual manifestation of diabetes mellitus.

    MEDICAL history: Type 2 diabetes mellitus for five years; unexplained 35-lb weight loss three years ago; Bell's palsy on right side many years ago. MEDICATIONS: glipizide, 10 mg/day. family history: Father died of leukemia at age 65; mother has kidney stones; no diabetes or neuromuscular disease. SOCIAL history: insurance salesman; heterosexual, promiscuous, uses condoms; smokes (25 pack years); does not drink. physical examination: Well-nourished, well developed, not in acute distress; had difficulty rising from a sitting position because of right lower extremity weakness. blood pressure, 154/74; pulse, 88; temperature, 36.6 degrees C; respiratory rate, 16. head, eyes, ears, nose, and throat: normal. neck: normal. heart: S4. Lungs: clear. abdomen: mildly obese. extremities: no cyanosis, clubbing, or edema; atrophy and weakness of right thigh and both calves; wide-based gait; able to walk on toes but not heels. Neurologic responses: cranial nerves intact; deep tendon reflexes, 1 symmetrically; plantar reflexes, flexor bilaterally. skin: macular rash in sun-exposed areas. LABORATORY FINDINGS: Hemoglobin, 13.2 gm/dL; mean corpuscular volume, 80 micron 3; white blood cell count, 7,200/mm3 (normal differential); platelet count, 137,000/mm3. serum: electrolytes, normal; blood urea nitrogen, 18 mg/dL; creatinine, 0.8 mg/dL; glucose, 308 mg/dL; total protein, albumin, liver enzymes, and creatine kinase, normal. urine: 1 glucose. Venereal disease test: nonreactive; hiv test: negative. DIFFERENTIAL diagnosis: dermatomyositis; heavy-metal poisoning; diabetic amyotrophy. HOSPITAL COURSE: The patient was given 50 mg/day of oral amitriptyline to alleviate the painful paresthesias and was switched to 20 U/day of subcutaneously injected neutral protamine Hagedorn (NPH) insulin to normalize the blood glucose level. Histologic studies of skin and muscle showed sun damage and neuropathic changes, respectively. There was no evidence of vasculitis. Screening for heavy-metal toxins produced negative results.
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2/33. metformin retention independent of renal failure in intestinal occlusion.

    metformin is eliminated by the kidneys, and metformin accumulation has always been noticed in oligo-anuric patients. We have reported an exception to the rule with the case of a metformin-treated patient having metformin accumulation contrasting with a mild increase in serum creatinine in the context of a volvulus of the sigmoid colon. This case prompted us to examine the association between intestinal occlusion and plasma metformin concentrations. For this purpose, we developed an experimental animal model of mechanical obstruction of the intestine. rats were pre-treated during 3 weeks via drinking solution at a dose of approximately 100 mg/kg/day of metformin. They underwent at day 0 either sham-operation (n=7) or operation (n=8) to place a plastic tube around the ileum near the ileocaecal valve. metformin administration was pursued on days 1, 2, and 3 giving a single dose of 100 mg/kg by intragastric gavage. Four days after the surgery, i.e. 24 h after the last metformin administration, the surviving intestinal obstructed rats (n=8) developed overt intestinal dilation but no biochemical abnormality compared to sham-operated animals (n=7; arterial lactate concentrations respectively 4.87 /- 0.63 mmol/l and 3.97 /- 0.30 mmol/l, NS, and serum creatinine concentrations 69.0 /- 1.7 micromol/l and 68.7 /- 1.9 micromol/l, NS). By contrast, there was a striking difference with regard to metformin concentrations, decreasing from 2.95 /- 0.94 mg/l at day 0 to 0.12 /- 0.03 mg/l at day 4 (p<0.001) in the sham-operated group but remaining unchanged (1.65 /- 0.76 mg/l and 1.61 /- 0.51 mg/l) in the operation group. In conclusion, this is the first experiment showing that intestinal occlusion may be responsible for metformin retention in the absence of renal failure. Whether this observation may be relevant to other drugs remains to be established.
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3/33. Fatal fetal outcome with the combined use of valsartan and atenolol.

    OBJECTIVE: To report a case of anhydramnios, pulmonary hypoplasia, very small placenta, and fetal death in a pregnancy complicated by chronic hypertension and diabetes mellitus that had been treated through the first 24 weeks of gestation with valsartan and atenolol. CASE SUMMARY: A 40-year-old Hispanic woman with well-controlled chronic hypertension and diet-controlled type 2 diabetes mellitus was treated with valsartan and atenolol until pregnancy was diagnosed at 24 weeks' gestation. An ultrasound examination revealed normal fetal growth and anatomy but anhydramnios (amniotic fluid index 0). Valsartan was discontinued, and amniotic fluid volume normalized within two weeks. Intrauterine fetal death was documented at 33 weeks' gestation. Labor was induced, with the delivery of a stillbom female fetus with small, hypoplastic lungs (weight 41% of expected) and an extremely small, 148-g placenta (weight 48% of the 10th percentile for gestational age). DISCUSSION: The use of valsartan, a selective angiotensin ii receptor antagonist (ARA), in human pregnancy has not been reported, but this class of agents would be expected to cause fetal toxicity similar to that observed with angiotensin-converting enzyme inhibitors. This toxicity includes reduced perfusion of the fetal kidneys, resulting in anuria, oligohydramnios, and subsequent pulmonary hypoplasia. The small hypoplastic lungs and very small placenta were probably a consequence of valsartan and atenolol combination therapy. CONCLUSIONS: Resolution of anhydramnios after discontinuing valsartan is evidence for ARA-induced fetal toxicity. The pulmonary hypoplasia observed in the stillbom infant was a direct result of the severe oligohydramnios. The cause of fetal death nine weeks later is uncertain, but because the woman's chronic hypertension and diabetes were well controlled, we believe the primary cause was chronic placental insufficiency resulting from the previous combination of valsartan and atenolol.
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4/33. Type I membranoproliferative glomerulonephritis in an hiv-infected individual without hepatitis c co-infection.

    Type I membranoproliferative glomerulonephritis (MPGN) is an uncommon manifestation of human immunodeficiency virus (hiv)-associated renal disease in patients co-infected with hepatitis c virus (HCV). We describe a case of Type I MPGN in an hiv-positive diabetic man with nephrotic-range proteinuria and renal insufficiency who was not co-infected with HCV. Tubuloreticular inclusions were present but there was no evidence for either cryoglobulinemia or cryoglobulin deposits in the kidney. This finding suggests that Type I MPGN may represent a reaction of the kidney to hiv independent of the effects of HCV co-infection. Clinical suspicion must be maintained for Type I MPGN in all hiv infected patients presenting with significant proteinuria regardless of HCV infection status.
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5/33. Celecoxib-induced acute interstitial nephritis.

    Data about the nephrotoxicity of selective cyclooxygenase-2 inhibitors are still evolving. Acute interstitial nephritis is a well-described complication of therapy with nonselective nonsteroidal anti-inflammatory drugs. We report a case of biopsy-proven acute interstitial nephritis in a 73-year-old diabetic woman, who had taken celecoxib for more than 1 year before presentation. She presented with clinical findings of subnephrotic proteinuria and acute renal failure that required dialysis. She recovered renal function with cessation of celecoxib therapy after 2 weeks. Other medications were reintroduced safely, without recurrence of renal failure. A kidney biopsy specimen showed acute interstitial nephritis with a prominent eosinophilic infiltrate in the interstitium. This case documents the occurrence of acute interstitial nephritis with celecoxib and emphasizes the need for continued vigilance and care in use of cyclooxygenase-2 inhibitors in high-risk patients.
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6/33. Renal cysts and diabetes syndrome linked to mutations of the hepatocyte nuclear factor-1 beta gene: description of a new family with associated liver involvement.

    BACKGROUND: Mutations in the hepatocyte nuclear factor (HNF)-1beta gene (TCF2) are responsible for a syndrome characterized by maturity-onset diabetes of the young, a nondiabetic renal disease, genital malformations, and liver dysfunction. methods: The HNF-1beta gene was screened for mutations in four members of an Italian family with early-onset, nonketotic diabetes or a familiar, nondiabetic renal disease and nonprogressive liver disorder. RESULTS: The genetic analysis revealed an already described nonsense mutation in codon 177 of HNF-1beta gene (R177X) in the four related subjects. Clinical features included diabetes in three of four patients, monolateral renal hypoplasia with cysts in the controlateral kidney in two patients, and bilaterally small hyperechoic kidneys without cysts in the other two patients. Renal function impairment was severe in one patient, requiring dialysis treatment, and mild in three. Three patients had nonprogressive liver dysfunction, with long-lasting enzyme alterations but no liver insufficiency or jaundice. CONCLUSION: HNF-1beta gene mutations are associated with a wide variability in severity and pattern of clinical symptoms within the same kindred regarding diabetes and renal impairment. Moderate liver dysfunction may be a so far overlooked component of the syndrome.
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7/33. Pseudomembranous candidosis in nephrotic syndrome: a case report.

    A 33-year-old male presented for evaluation of several large, recently discovered white oral lesions of unknown duration. Clinical examination revealed multiple white plaques on the soft palate, uvula, buccal mucosa, and tongue. These lesions could be wiped away, leaving an erythematous base. The lesions were asymptomatic, and the patient did not report difficulty in swallowing. The patient's medical history was noteworthy for several significant diagnoses within the previous 6 months: type 2 diabetes mellitus, mild systolic hypertension, gastroesophageal reflux disease, and adult idiopathic nephrotic syndrome, determined by kidney biopsy to be caused by focal segmental glomerulosclerosis. A provisional diagnosis of pseudomembraneous candidosis was made, and the patient responded to a 14-day course of clotrimazole, administered in 10-mg troches, five times a day. Management of nephrotic syndrome predisposes patients to recurrent fungal infections, and the disease has implications for the selection of systemic antifungal agents.
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8/33. Emphysematous pyelonephritis: no longer a surgical disease?

    Emphysematous pyelonephritis is a rare, life-threatening infection of the kidney characterized by the presence of gas within the renal parenchyma, the renal collecting system and the perinephric tissue. It usually develops in diabetic patients and often presents abruptly with bacteraemia, septic shock and acute renal failure. diagnosis can be delayed because the symptoms mimic a classical upper urinary tract infection. Aggressive management, including parenteral antibiotic therapy, treatment of septic shock and control of the glycaemia, is mandatory. Immediate nephrectomy has been considered to be essential to increase the chance of survival. Recently, percutaneous drainage has been reported as a kidney-saving and life-saving alternative to surgery. We present a case of severe emphysematous pyelonephritis in which there was full recovery after antibiotic treatment combined with temporary percutaneous drainage. The therapeutic options in this rare, life-threatening condition are discussed.
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9/33. Does type 2 diabetes mellitus delay renal failure in autosomal dominant polycystic kidney disease?

    Autosomal dominant polycystic kidney disease (ADPKD) is a common renal disease without an effective therapeutic intervention to delay renal failure. Within kindreds, renal dysfunction often develops at a similar age in affected individuals, although there are known modifying factors. Two kindreds with ADPKD have shown a striking pattern of delayed onset of renal insufficiency in those individuals also suffering from type 2 diabetes mellitus. Eight nondiabetic patients with ADPKD had onset of dialysis or renal death at ages 38-52 years, (mean /- SEM 46 /- 1.9, n = 7) as compared with four diabetics who started dialysis or are still off dialysis at the age of 61 /- 2.8 years (p < 0.01). Two of the four diabetics still have reasonable renal function at age 61 and 66. The diabetes was diagnosed at age 32 /- 2 years and was treated with oral hypoglycemics for 19 /- 2 years before institution of insulin. Cardiovascular disease dominated the clinical picture in the diabetics. In conclusion, onset of renal failure in ADPKD was delayed for over 15 years in individuals who also suffered from type 2 diabetes mellitus, in two ADPKD kindreds. Possible mechanisms are discussed, including glibenclamide inhibition of the cystic fibrosis transmembrane conductance regulator. The striking delay associated with type 2 diabetes mellitus in ADPKD induced renal failure should be evaluated further.
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keywords = kidney disease, kidney
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10/33. Combined pancreas and kidney transplantation in a lean type 2 diabetic patient. Effects on insulin secretion and sensitivity.

    BACKGROUND/AIMS: pancreas transplantation is an established method of treating Type 1 diabetes. It was our aim to test the consequences of pancreas transplantation in a Type 2 diabetic patient by determining insulin secretion and sensitivity before and after surgery. patients AND methods: A female patient with Type 2 diabetes and end-stage nephropathy was treated with combined pancreas and kidney transplantation. Before surgery and at 4 weeks, 6 months and 2 years afterwards, insulin sensitivity was measured using hyperinsulinemic euglycemic clamps and insulin secretion was quantified after oral glucose or intravenous glucagon challenges. RESULTS: The patient was insulin resistant before surgery (glucose infusion 4.6 mg. kg (-1). min (-1), normal range 6.4 /- 0.5 mg.kg( -1). min (-1). Insulin sensitivity declined further after transplantation (1.4 and 3.0 mg. kg -1. min -1 after 4 weeks and 6 months, respectively), but improved to 5.4 mg. kg (-1). min (-1) after 2 years. Insulin secretion was greatly impaired before surgery. Insulin and c-peptide responses after oral glucose and intravenous glucagon increased into the normal range from 6 months after surgery onwards and oral glucose tolerance remained non-diabetic (IGT). CONCLUSIONS: insulin resistance is first aggravated after pancreas transplantation, probably due to immunosuppressive treatment including glucocorticoids, but improves on the long term. The initially impaired insulin secretion from the transplant may also be explained by the action of glucocorticoids or by transient and reversible organ damage.
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