The Effect of PPAR gamma2 Pro12Ala Polymorphism on Diabetic Nephropathy in Type 2 Diabetes / 대한신장학회잡지

BACKGROUND: Recently, the PPAR gamma2 Pro12Ala polymorphism has been associated with type 2 diabetes and diabetic nephropathy. In the present study, we investigated the association between Pro12Ala polymorphism and diabetic nephropathy in korean subjects. METHODS: A total of 180 patients with type 2 diabetes and 100 normal controls were enrolled in this studies. Screening for mutation at codon of PPAR gamma2 were carried out by PCR-RELP analysis. Also, we measured important covariables, such as duration of diabetes, blood pressure, renal function and serum lipids. RESULTS: In PCR-RELP, it showed that there were no difference in the PPAR gamma2 genotype frequencies between diabetic subjects (Pro/Pro: 80.5%, Pro/Ala: 19.5%) and normal controls (88%, 12%). However, it showed that there were significant difference in the PPAR gamma2 genotype frequencies between diabetic subjects with nephropathy (Pro/Pro: 74.5%, Pro/Ala: 25.5%) and diabetic subjects without nephropathy (87.8%, 12.2%) (p=0.040). In diabetic subjects, Pro/Ala genotypes were significantly different from Pro/Pro regarding serum creatinine, 24 hour proteinuria, systolic pressure, and LDL-cholesterol. In diabetic nephropathy, genotypes with Pro/Ala significantly increased serum creatinine (2.7+/-0.41 vs 1.7+/-0.68 mg/dL), 24hour urine protein (median+-SE: 1.9+/-1.02 vs 0.9+/-0.44 g/day), systolic pressure (161+/-27.8 vs 152+/-32.4 mmHg), LDL cholesterol (134+/-30.4 vs 125+/-20.0 mg/dL), and triglyceride (151+/-86.5 vs 135+/-60.9 mg/dL) than genotypes with Pro/Pro. CONCLUSION: Our results suggested that Pro12Ala Polymorphism of the PPAR gamma2 gene may be associated with diabetes with nephropathy in korean patients.

A case of carbamazepine induced acute interstitial nephritis / 대한내과학회지

Acute interstitial nephritis often caused by drugs and infection. Interstitial nephritis by drugs is a kind of idiosyncratic reaction and is caused independently of dosage. This disease developed within several days or weeks after taking medicine but improved if discontinue medication. Adrenocortical hormone may shorten the period of disease if renal dysfunction continued. Acute interstitial nephritis by carbamazepine that is used for epilepsy cure is rarely reported. A 49-year-old male was admitted to our hospital because of skin rash and decreased urine volume which developed 10 days ago. Patient was diagnosed intracranial hemorrhage 6 months ago and was taking carbamazepine because of tingling sensation to lower extremity before 2 months. At admission, blood pressure 120/80 mmHg, hemoglobin 12.6 g/dL, WBC 232,000/mm3, eosinophil count 2,790/mm3, platelet 166,000/mm3. Urine findings indicated protein 1+, blood 2+ and eosinophil was observed in microscopic examination. Abdominal sonography showed increase of both kidney size, shade of renal cortex and Resistance index (RI). Renal biopsy showed inflammatory cell consisted of lymphocyte, eosinophil in parenchyme was seen with tubular necrosis partially. Renal function was improved after carbamazepine withdrawal and adrenocortical hormone medication.

A case of nephrocalcinosis with primary aldosteronism / 대한내과학회지

Primary aldosteronism is defined as hypertension, hypokalemia, increased serum aldosteron, decreased serum renin activity. It has been known that prolonged hypokalemia, renal cyst formation and impairment of renal function. However, nephrocalcinosis associated with primary aldosteronism is rarely reported. A 31-year-old male was admitted to our hospital because of abdominal pain and uncontrolled hypertention which developed 2 years earlier. At admission, blood pressure 180/100 mmHg. Biochemical findings indicated sodium 146 mEq/L, potassium 2.3 mEq/L, BUN 8.2 mg/dL, creatinine 1.1 mg/dL, calcium 10.7 mg/dL, phosphate 5.7 mg/dL, magnesium 1.8 mg/dL. Twenty-four hour urine collection indicated sodium 108 mEq, potassium 32 mEq, calcium 75 mg, phosphate 72 mg, magnesium 8.0 mg. The hormone study revealed PTH 22.7 pg/mL (normal: 9~55 pg/mL), ACTH 8 pg/mL (normal: 6~56.7 pg/mL), aldosterone 51.0 ng/dL (normal: 1~16 ng/dL), plasma renin activity below 0.01 ng/mL/hr (normal: 0.15~233 ng/mL/hr). Abdominal sonography showed homogenous increased medullary echoes and multiple calcification. The abdomen CT showed adrenal mass (1 x 1 cm) consistent with adrenal tumor. Adrenalrectomy was performed on the 16th hospital day and clinical symptoms, blood pressure and hypokalemia improved shortly after operation.

Chronic hyponatremia of Sheehan's syndrome / 대한내과학회지

Sheehan's syndrome has been attributed to ischemic damage of the pituitary gland or hypothalamic-pituitary stalk during the peripartum period. Well-described clinical features of Sheehan`s syndrome include hypothyroidism, growth hormone deficiency, hypogonadism, hypoprolactinemia, adrenal insufficiency, and different sodium and water disturbance. The occurrence of sodium and water disturbances associated with Sheehan`s syndrome depends on the degree of pituitary damage, time of onset since the initial pituitary insult, and concurrent medical conditions that also may play a role in sodium and water balance. Chronic hyponatremia is the most common presentation of altered sodium levels in patients with Sheehan`s syndrome. The chronic nature of the presenting hyponatremia suggests more subtle changes of panhypopituitarism or better adaptive mechanism. Although controversial, another mechanism proposed for hyponatremia in the chronic setting involves alternation in the renin-angiotensin/aldosterone system with resulting sodium wasting. We presented a patient with Sheehan`s syndrome associated with hyporeninemic hypoaldosteronism and hyponatremia 53 years old women, who had 4th baby delivery with severe blood loss about 25 years ago, was admitted to hospital because of general weakness. The patient was diagnosis Sheehan`s syndrome with hyponatremia. In addition, we performed hormonal study to find cause of hyponatremia. The results were hypopituitarism and hyporeninemic hypoaldosteronism. Hyponatremia was corrected by hormonal therapy (glucocorticoid,synthyroid,estrogen). The patient felt well-being sensation and was followed up the out-patient department.