To evaluate angiotensin-converting enzyme (ACE) gene insertion/deletion polymorphism in nephrotic syndrome, 85 patients (minimal-change nephrotic syndrome, MCNS: 55 cases; focal segmental glomerulosclerosis, FSGS: 30 cases) and 61 control subjects were examined. The distribution of ACE genotype in the control group was II 44%, ID 41 % and DD 15 %. The distribution of ACE genotypes in MCNS was similar to that in controls. However, the distribution of ACE genotypes in FSGS was markedly different from those of MCNS. The DD genotype was more frequent (p < 0.05) in FSGS than in MCNS. Patients with the DD genotype tended to present clinical symptoms at an earlier age. They also showed a lower responsiveness to corticosteroid therapy and a higher incidence of chronic renal failure than those with other genotypes. Our results indicate that the ACE DD genotype in FSGS may be a risk factor for the poor responsiveness to steroid therapy and the development of chronic renal failure.

D-Lactic acidosis has been well documented in ruminants. In humans, D-lactic acidosis is very rare, but D-lactic acidosis may be more common than generally believed and should be looked for in a case of metabolic acidosis in which the cause of acidosis is not apparent. The clinical presentation of D-lactic acidosis is characterized by episodes of encephalopathy and metabolic acidosis. The entity should be considered as a diagnosis in a patient who presents with metabolic acidosis accompanied by high anion gap, normal lactate level, negative Acetest, history of short bowel syndrome or malabsorption, and characteristic neurologic manifestations. Low carbohydrate diet, bicarbonate treatment, rehydration, and oral antibiotics would be helpful in controlling symptoms.

ObjectivesTo investigate the renal function and hemodynamic changes in obesity and hyperinsulinemia which are characteristics of type II diabetes.MethodsStudies were carried out in two groups of female Zucker rats. Group 1 rats were obese Zucker rats with hereditary insulin resistance. Group 2 rats were lean Zucker rats and served as controls. In comparison with lean Zucker rats, obese Zucker rats exhibited hyperinsulinemia but normoglycemia. Micropuncture studies and morphologic studies were performed in these rats.ResultsFunctional studies showed that obese Zucker rats exhibited increases in kidney weight and GFR(obese Zucker, 1.23±.07)ml/min; lean Zucker, 0.93±.03ml/min). Micropuncture studies revealed that the increase in GFR in obese Zucker rats was attributable to the increases in the single nephron plasma flow rate and glomerular transcapillary hydraulic pressure. The glomerular ultrafiltration coefficient was the same in both groups. Morphologic studies revealed that the increase in GFR in obese Zucker rats was associated with an increase in glomerular volume.ConclusionsThese results suggest that obesity and hyperinsulinemia, which are the characteristics of type II diabetes, can be associated with glomerular hyperfiltration and glomerular capillary hypertension.

The family of cyclins and cyclin-dependent kinases (CDKs) are important participants in the regulation of eukaryotic cell cycle. Our purpose was to examine temporal expressions of cyclins and CDKs during renal development and compensatory growth. During embryonic development the mRNA levels of all cyclins were high, and after birth their levels decreased at different rates. G2 and M phase cyclins, cyclin A and B, decreased immediately after birth. G1 and S phase cyclins, cyclins D1, D2, D3, and E, were observed during all stages of development and maintained almost constant levels until seven days after birth. They decreased thereafter and expressed very low levels during the adult period. The protein levels of cdc2, CDK2, and proliferating cell nuclear antigen (PCNA) were high during embryonic renal development and slowly decreased after birth. Their levels were very low during the youth and adult periods. Levels of CDK4 protein were high and did not change during renal development. Compensatory hypertrophic renal growth (CHRG) induced by unilateral nephrectomy (Unx) did not increase any cyclins, CDKs or PCNA. Subtotal nephrectomy (Snx) did not increase any cyclins or CDKs in remaining viable renal tissue (RVRT). However, Snx increased PCNA in RVRT. An immunohistochemical study revealed that PCNA was induced in a limited area adjacent to ischemic areas. Interestingly, Western blot analysis of protein extracts from RVRT showed the induction of a new 40 kDa protein that cross-reacted with the cyclin D3 antibody. These findings suggest that the marked reductions in mitotic cyclins may be associated with the withdrawal of renal cell cycle after birth. In addition, expressions of cyclins and CDKs did not change in the adult kidney during active phase of compensatory hypertrophic growth.

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The anion gap in the serum is useful in the interpretation of acid-base disorders and in the diagnosis of other conditions. In the early 1980s, ion-selective electrodes for specific ionic species were introduced for the measurement of serum electrolytes. This new method has caused a shift of the anion gap from 12±4 mEq/L down 6±3 mEq/L. It is worthy for clinicians to understand the range of normal anion gap and the measuring methods for serum sodium and chloride in the laboratories that support their practice. While an increase in the anion gap is almost always caused by retained unmeasured anions, a decrease in the anion gap can be generated by multiple mechanisms.

Unilateral renal cystic disease (URCD) is a distinct entity that is one of the renal cystic diseases. The clinical importance of URCD is to make a differential diagnosis from autosomal dominant polycystic kidney disease (ADPKD), multicystic dysplastic kidney, multilocular cystic renal neoplasm, and simple cysts. To confirm the diagnosis and to rule out asynchronous ADPKD requires long-term follow up, especially in younger patients.

Analysis of the five different serum isoenzymes of lactate dehydrogenase (LDH) is of great value in the differential diagnosis of various diseases. In order to investigate the changes of serum LDH isoenzymes in several renal diseases, 44 patients with Korean hemorrhagic fever, 10 patients with chronic renal failure, 10 patients with nephrotic syndrome, and 15 healthy subjects were studied. The isoenzymes of LDH were determined by the Helena LDH isoenzyme electrophoresis procedure. LDHl was 22.3 ± 2.8, LDH2 29.4 ± 5.1, LDH3 20.8 ± 4.5, LDH4 9.0 ± 2.7 and LDH5 8.8 ± 3.2 mU/ml in healthy subjects. In patients in the oliguric stage of Korean hemorrhagic fever, LDHl was 63.4 ± 28.5, LDH2 99.7 ± 40.7, LDH3 107.5 ± 39.0, LDH4 41.9 ± 32.8 and LDH5 37.2 ± 26.3 mU/ml, while LDHl was 23.8 ± 11.7, LDH2 38.9 ± 14.6, LDH3 36.0 ± 18.7, LDH4 13.8 ± 13.0 and LDH5 12.7 ± 7.6 mU/ml in nonoliguric patients. In patients with chronic renal failure LDH1 was 33.2 ± 10.8, LDH2 41.9 ± 13.3, LDH3 27.7 ± 8.5, LDH4 12.1 ± 6.2 and LDH5 12.3 ± 5.8 mU/ml. In patients with nephrotic syndrome, LDH1 was 25.1 ± 4.3, LDH2 33.5 ± 4.9, LDH3 23.1 ± 6.2, LDH4 8.4 ± 3.7 and LDH5 8.4 ± 3.4 mU/ml. In summary, LDH3 activity was elevated in the oliguric stage of Korean hemorrhagic fever and LDH2 was elevated in chronic renal failure; those values were correlated with the BUN level.