Heavy proteinuria with or without features of nephrotic syndrome is associated with many primary and systemic diseases. For diabetic patients, distinguishing nondiabetic renal disease (NDRD) from diabetic nephropathy (DN) is important in choosing treatment modalities and determining renal prognosis. However, clinical relevance of heavy proteinuria is inconsistent with clinical DN assessments. This study investigated the clinicopathological features and renal outcomes of DN and NDRD in type 2 diabetic patients with nephrotic-range proteinuria.We enrolled 220 cases of type 2 diabetic patients who underwent renal biopsy. They were grouped according to the presence of nephritic-range proteinuria and pathological features. Baseline characteristics, laboratory findings, types of pathological diagnosis, and renal outcomes were analyzed in patients with heavy proteinuria.Upon kidney biopsy, 129 patients (58.6%) showed nephritic-range proteinuria. Patients with heavy proteinuria (an average urine protein-to-creatinine ratio of 10,008 ± 7307 mg/gCr) showed lower serum albumin levels and higher total cholesterol levels, but did not show any difference in age, duration of diabetes, renal function, or the presence of retinopathy compared with those with mild-to-moderate proteinuria (an average urine protein-to-creatinine ratio of 1581 ± 979 mg/gCr). Renal biopsy revealed that the prevalence of NDRD was 37.2% in patients with heavy proteinuria, which was significantly lower than that in patients with mild-to-moderate proteinuria (63.7%). The most common pathological types of NDRD were membranous nephropathy (41.7%), IgA nephropathy (14.6%), and minimal change disease (10.4%). NDRD patients showed lower prevalence of diabetic retinopathy and better kidney function irrespective of proteinuria. Immunosuppressive treatment was administered more frequently in patients with heavy proteinuria (56.3%) compared with patients with mild-to-moderate proteinuria (20%) because of the pathological differences according to the amount of proteinuria. Renal outcomes were significantly worse in patients with DN than in patients with NDRD.DN patients with heavy proteinuria exhibited different prevalence of NDRD and worse prognosis. Renal biopsy in type 2 diabetic patients should be more extensively considered to accurately diagnose NDRD, guide further management, and predict renal outcomes, especially in patients with nephrotic-range proteinuria.

This study aimed to assess the effects of different dialysate bicarbonate concentrations in correcting acid-base imbalance in 53 stable hemodialysis patients in a university-hemodialysis unit. Three different bicarbonate concentrations were assigned, i.e. 25 mEq/L in 10, 30 mEq/L in 30, and 35 mEq/L in 13 patients. Blood gas analyses from arterial line blood samples before and after dialysis in the mid-week were performed for the determination of pH and serum bicarbonate (HCO3-) concentration. The mean values of predialysis arterial HCO3- were mildly acidotic in all 3 groups, but not significantly different among them, whereas those of post-dialysis arterial HCO3- were alkalotic, especially in the group of 35 mEq/L as compared with the other two groups. The mean blood pH was not significantly different among the 3 groups. As expected, there was a positive correlation between pre-dialysis pH and post-dialysis pH (r=0.45, p=0.001), and pre-dialysis HCO3- and post-dialysis HCO3- (r=0.58, p=0.000), but with a negative correlation between pre-dialysis HCO3- and the increment of intradialytic HCO3- following hemodialysis (r=-0.46, p=0.001). In conclusion, this study shows that the impact of conventional dialysate bicarbonate concentrations ranging from 25 to 35 mEq/L is not quite different on the mild degree of predialysis acidemia, but the degree of postdialysis alkalemia is more prominent in higher bicarbonate concentrations. Base supply by hemodialysis alone does not seem to be the main factor to determine the predialysis acidosis in end-stage renal disease patients on chronic maintenance hemodialysis.

We report a rare case of the concurrent manifestation of central diabetes insipidus (CDI) and type 2 diabetes mellitus (DM). A 56 year-old man was diagnosed as a type 2 DM on the basis of hyperglycemia with polyuria and polydipsia at a local clinic two months ago and started an oral hypoglycemic medication, but resulted in no symptomatic improvement at all. Upon admission to the university hospital, the patient's initial fasting blood sugar level was 140 mg/dL, and he showed polydipsic and polyuric conditions more than 8 L urine/day. Despite the hyperglycemia controlled with metformin and diet, his symptoms persisted. Further investigations including water deprivation test confirmed the coexisting CDI of unknown origin, and the patient's symptoms including an intense thirst were markedly improved by desmopressin nasal spray (10 µg/day). The possibility of a common origin of CDI and type 2 DM is raised in a review of the few relevant adult cases in the literature.

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This is a case of a sudden cardio-pulmonary arrest in a 29 year-old female, which occurred immediately after a large bolus infusion of propofol (100 mg) intravenously during dilatation and curettage. The arrest suddenly occurred, and the patient was eventually transferred to our emergency room (ER) on cardiopulmonary resuscitation. At that time, severe hyperkalemia up to 9.1 mEq/L and ventricular fibrillation were noted. Resuscitation in ER worked successfully with conversion of electrocardiograph to sinus rhythm, but this patient expired unfortunately. On view of this acute event immediately after the bolus injection of propofol accompanied without other identified causes, severe hyperkalemia induced by propofol was strongly assumed to be the cause of death. To our understanding with the literature survey, propofol as a cause of hyperkalemia has not been well described yet. Through this case, the relationship as a cause and an effect between propofol and hyperkalemia is suggested.