The foremost step in the initial clinical management of hyperkalemia is to decide whether a hyperkalemic patient requires immediate treatment to avoid a life-threatening situation (serum potassium concentration >6.0 mEq/l and EKG changes). When the decision for urgent treatment of hyperkalemia is based on EKG changes, an important caveat for clinicians is that absent or atypical EKG changes do not exclude the necessity for immediate intervention. Once an urgent situation has being handled with intravenous push of a 10% calcium salt, the initiation of short-term measures can be launched by either a single or combined regimen of the three agents that cause a transcellular shift of potassium – insulin with glucose, β₂-agonist (albuterol), and NaHCO₃. As the first choice among these available options, we favor an intravenous bolus of 10 units of insulin with 50 ml of 50% glucose alone or in combination with 10–20 mg of albuterol by nebulizer. These can be repeated as required until the institution of hemodialysis. The combination of insulin with glucose and NaHCO₃ as an another option needs further clarification for its additive effects. However, NaHCO₃ has lost its favor because of its poor efficacy as a potassium-lowering agent when used alone. The next step is to remove potassium from the body – diuretics (furosemide), cation exchange resin (kayexelate) with sorbitol, and dialysis (preferably hemodialysis). The final important step for the managements of hyperkalemia is a long-term plan to prevent its recurrence or worsening. In addition to every effort to elucidate underlying causes and pathophysiologic mechanisms for hyperkalemia, an extensive search must be made to uncover overt or sometimes covert medications that may have led to the development of hyperkalemia. Furthermore, one must obtain detailed dietary and medical history of hyperkalemic patients.

Because of increases in the elderly population and diabetic patients, the proportion of elderly among dialysis patients has rapidly increased during the last decades. The mortality and morbidity of these elderly dialysis patients are obviously much higher than those of young patients, but large analytic studies about elderly dialysis patients' characteristics have rarely been published. The registry committee of the Korean Society of Nephrology has collected data about dialysis therapy in Korea through an Internet online registry program and analyzed the characteristics. A survey on elderly dialysis patients showed that more than 50% of elderly (65 years and older) patients had diabetic nephropathy as the cause of end-stage renal disease, and approximately 21% of elderly dialysis patients had hypertensive nephrosclerosis. The proportion of elderly hemodialysis (HD) patients with native vessel arteriovenous fistula as vascular access for HD was lower than that of young (under 65 years) HD patients (69% vs. 80%). Although the vascular access was poor and small surface area dialyzers were used for the elderly HD patients, the dialysis adequacy data of elderly patients were better than those of young patients. The laboratory data of elderly dialysis patients were not very different from those of young patients, but poor nutrition factors were observed in the elderly dialysis patients. Although small surface area dialyzers were used for elderly HD patients, the urea reduction ratio and Kt/V were higher in elderly HD patients than in young patients.

The purpose of this study is to evaluate the effect of haemodialysis on perfused vessel density, choroidal thickness (CT), and retinal thickness in end-stage renal disease (ESRD) using swept-source optical coherence tomography angiography (SS-OCTA). We studied twenty-nine eyes of 29 ESRD patients by ophthalmologic examination and SS-OCTA before and after haemodialysis. The colour-coded perfusion density maps were generated and perfused vessel density was calculated. Changes in systemic and other ocular parameters such as retinal and choroidal thickness were measured and analysed. Total perfused vessel density decreased significantly after haemodialysis in the choriocapillaris; it was not significantly different in the superficial capillary plexus (SCP) and the deep capillary plexus (DCP). Total CT decreased significantly, but total retinal thickness was not significantly different. There was no significant correlation between choriocapillaris perfused vessel density and CT. The reduction in choriocapillaris perfused vessel density correlated with the decrease in systolic and mean arterial blood pressures. The decrease in CT correlated with the ultrafiltration volume. There were no significant systemic and ocular factors affecting change in retinal thickness and perfused vessel density of SCP and DCP. This is the first study to assess the effect of haemodialysis on blood flow changes using SS-OCTA; changes may be more prominent in the choroidal compared to the retinal layer.

Background. Renin-angiotensin system (RAS) blockades, angiotensin converting enzyme inhibitors (ACEIs) and angiotensin II receptor blockers (ARBs) are well accepted for the cardiorenal-protective benefits added to antihypertensive effects in chronic kidney diseases (CKD), but associated with an increased risk of hyperkalaemia. However, few studies have investigated the effect of RAS blockades on serum potassium in dialysis patients. Methods. Hyperkalaemia associated with RAS blockades by ACEI and/or ARB was evaluated in 69 patients on maintenance haemodialysis, who underwent a three-period crossover study in four groups (no exposure to RAS blockades, ACEI or ARB alone and ACEI plus ARB treatments), lasting one month in each period. Results. Sixty-two patients completed this prospective 3-month study, and no one stopped the study because of the development of hyperkalaemia and/or complications. Mean serum K was similar among the four periods (no exposure, 5.54 AE 0.67 mmol/l; ACEI alone, 5.54 AE 0.75 mmol/l; ARB alone, 5.50 AE 0.66 mmol/l; ACEI þ ARB combination, 5.42 AE 0.66 mmol/l) and was also equal when compared between the two groups with and without exposure to RAS blockades (5.48 AE 0.68 vs 5.54 AE 0.67 mmol/l, P ¼ NS). The incidence of severe hyperkalaemic episodes (>6.0 mmol/l) upon monthly predialysis serum K determination was 25.8% with no exposure to RAS blockades, 29.8% for ACEI alone, 19.6% for ARB alone and 17.7% for ACEI þ ARB combination without statistically significant differences among the four periods (P ¼ NS). Among covariables, the degree of Kt/V, intakes of other medications interfering with potassium homeostasis and diabetes mellitus did not result in any significant hyperkalaemic changes during the 3-month study period except anuric patients compared with non-anuric patients (5.58 AE 0.69 vs 5.19 AE 0.65 mmol/l, P < 0.001). Conclusion. Neither monotherapy (ACEI or ARB) nor combination therapy (ACEI plus ARB) is associated with the additional risk of hyperkalaemia in patients on maintenance haemodialysis. However, those patients with anuria on RAS blockades warrant the cautious monitoring of serum K to prevent hyperkalaemia.

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.

Arterial thrombosis is relatively rare compared with venous thrombosis in nephrotic syndrome. However, the assessment of its pathogenesis and risk factors in individual patient with nephrotic syndrome is necessary to allow appropriate prophylactic management because it is a potentially serious problem. Hereby, with review of the literature, we report a case of a 53 yr-old man with cerebral infarction associated with nephrotic syndrome due to focal segmental glomerulosclerosis during the course of treatments with diuretics and steroid. It reveals that the hypercoagulable state in nephrotic syndrome can be associated with cerebral infarction in adults. Prophylactic anticoagulants can be considered to reduce the risk of serious cerebral infarction in nephrotic patients with risk factors such as severe hypoalbuminemia and on diuretics or steroid treatment, even in young patients regardless of types of underlying glomerular diseases.

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.