Metabolic acidosis was shown to correlate with deterioration of renal function in patients with rhabdomyolysis. The present study was aimed to investigate whether the changes of type 3 Na+/H+ exchanger (NHE3), type 1 Na+/HCO3- cotransporter (NBC1), and Na+,K+-ATPase α1 subunit may play a role in the pathogenesis of metabolic acidosis in glycerol-induced experimental rhabdomyolysis. Male Sprague-Dawley rats were deprived of fluid intake for 24 hours, and then were injected with 50% glycerol in normal saline (10 mL/kg, intramuscularly). At 24 hours after the glycerol injection, rats were sacrificed by decapitation. Control rats were injected with normal saline. The protein expression of NHE3, NBC1 and Na+,K+-ATPase α1 subunit was determined in the cortex of the kidney by immunoblotting and immunohistochemistry. Following the treatment of glycerol, creatinine clearance was significantly decreased, and high anion gap metabolic acidosis developed. In the experimental group, the expression of Na+,K+-ATPase α1 subunit was significantly decreased in the cortex of the kidney. On the contrary, the expression of NHE3 and NBC1 was significantly increased. Immunohistochemical analyses confirmed the immunoblotting data. In conclusion, the coordinate up-regulation of NHE3 and NBC1 may play an adaptive role against the metabolic acidosis in glycerol-induced rhabdomyolysis.

• Rhabdomyolysis
• Metabolic acidosis
• Type 3 Na+/H+ exchanger
• Type 1 Na+/HCO3- cotransporter

Renal handling of uric acid mainly occurs in the proximal tubule, and bidirectional transport of urate may involve apical absorption via the urate-anion exchanger (URAT1) and basolateral uptake via organic anion transporters (OAT1 and OAT3). In rat kidneys, we investigated whether the protein abundance of URAT1, OAT1, and OAT3 is affected by the increase in uric acid intake. Male Sprague-Dawley rats were randomly divided into control and uric acid-supplemented groups, and uric acid-supplemented rats were given 1.75 g of uric acid per 180 g body weight per day for 8 days. After the animal experiment, kidneys were harvested and semi-quantitative immunoblotting was carried out from cortical homogenates using polyclonal peptide-derived antibodies to URAT1, OAT1, and OAT3. Serum uric acid level showed an increasing tendency in the uric acid-supplemented rats compared with control rats, whereas urinary uric acid excretion was not significantly different between the uric acid-supplemented rats and control rats. URAT1 protein abundance in cortical homogenates was not significantly different between the uric acid-supplemented rats and control rats. However, OAT1 protein abundance was significantly increased in the uric acid-supplemented rats compared with the control rats. OAT3 protein abundance was not significantly different between the uric acid-supplemented rats and control rats. In conclusion, OAT1 may have a regulatory role in response to the increase in uric acid intake in the rat kidney. The up-regulation of OAT1 would exert stimulation of urinary uric acid excretion and might contribute to protection from hyperuricemia.

• Urate-anion exchanger
• Organic anion transporter
• Uric acid
• Dietary intake
• Rat

This study aimed to examine whether the expression of major prostaglandin E2 (PGE2) synthesis enzyme, cyclooxygenase-2 (COX-2), is changed in the kidneys of the rats with lithium-induced nephrogenic diabetes insipidus (Li-NDI). Sprague-Dawley rats treated with lithium for 4 weeks were used as the NDI model and expression of renal COX-2 was determined by immunoblotting and immunohistochemistry. In Li-NDI where urine output was markedly increased and urine osmolality was significantly decreased, COX-2 expression in the inner medulla was decreased (28% of control), while it increased 18-fold in the cortex and outer medulla. Consistent with this, labeling intensity of COX-2 in macula densa region was increased, whereas it was decreased in the interstitial cells in the inner medulla, indicating a differential regulation of COX-2 between the cortex and inner medulla in Li-NDI. Accordingly, urinary PGE2 excretion was significantly increased in Li-NDI. In conclusion, there is a differential regulation of COX-2 between cortex and inner medulla in Li-NDI and urinary PGE2 excretion is increased in Li-NDI, possibly due to an increased renal production. This may suggest that increased renal production of PGE2 could play a role in modulating water reabsorption in the renal collecting duct in Li-NDI.

• Aquaporins
• Cyclooxygenase-2
• Lithium
• Prostaglandins

Protein kinase C (PKC) plays an important role not only in signal transduction mechanisms in various biological processes, but also in the regulation of growth and differentiation during development. We studied the classical PKC α, βⅠ, βⅡ and γ, with regard to their expression in adult and developing rat kidney. PKCα appeared in the ureteric bud at embryonic day (E) 16, and the proximal and distal anlage at E18. After birth, the immunoreactivity of PKCα gradually decreased. In adult, PKCα was expressed intensely in the connecting tubule (CNT), the collecting ducts (CD) and the renal corpuscle, and weakly in the proximal and distal tubules. PKCβⅠ appeared in the ureteric bud at E16, and the proximal anlage at E18. After birth, the immunoreactivity of PKCβⅠ gradually disappeared from the CD and proximal tubule. In adult, PKCβⅠ was expressed in the intercalated cells of the CNT and cortical CD, the proximal straight tubule, and the renal corpuscle. PKCβⅡ appeared in distal anlage at E18, and increased markedly after birth. In the CD, PKCβⅡ immunoreactivity appeared after birth. In adult, PKCβⅡ was expressed in the distal tubule, the CNT and the CD. The immunoreactivity for PKCγ appeared only in the proximal anlage at E18, and increased temporally around the time of birth. However, no immunoreactivity for PKCγ was observed in adult rat kidney. These results indicate that classical PKC isoforms appear to play a role in the regulation of various renal functions and differentiation within specific functional units of the uriniferous tubule in rat kidney.

• Protein kinase C
• Development
• Kidney

The present study was aimed at investigating the role of type Ⅱ 11β-hydroxysteroid dehydrogenase (Ⅱβ-HSD Ⅱ) in the development of hypertension. Two-kidney, one-clip (2K1C), deoxycorticosterone acetate (DOCA)/salt, or NG-nitro-L-arginine methyl ester (L-NAME) hypertension was induced in male Sprague-Dawley rats. Four weeks later, the expression of 11β-HSD ⅡmRNA was determined in the kidney by Northern blot analysis. The plasma level of aldosterone was measured by radioimmunoassay. In 2K1C hypertension, the expression of 11β-HSD Ⅱ was decreased in the clipped kidney and increased in the non-clipped kidney. The expression was increased in the remnant kidney of DOCA/salt hypertension, while decreased in the kidneys of L-NAME hypertension. The plasma level of aldosterone was increased, decreased, and remained unchanged in 2K1C, DOCA/salt, and L-NAME hypertension, respectively. The down-regulation of 11β-HSD Ⅱ may contribute to the sodium retention, thereby increasing the blood pressure in 2K1C and L-NAME hypertension. On the contrary, the up-regulation in DOCA/salt hypertension may play a compensatory role to dissipate the sodium retention.

• Type 2 11β-hydroxysteroid dehydrogenase
• Kidney
• Hypertension

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 academia, 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.

• Acid-base imbalance
• Hemodialysis
• Bicarbonate dialysate

Hypokalemia is a frequent problem in patients on continuous ambulatory peritoneal dialysis (CAPD) and is affected by multiple factors. To evaluate factors associated with hypokalemia. we studied 68 patients on maintenance CAPD treatment for at least six months, In univariate analysis, patients with hypokalemia were associated with older age and the presence of diabetes mellitus. Serum albumin, calcium-phosphate product, triglyceride, body mass index, protein nitrogen appearance, and lean body mass assessed by creatinine kinetics were significantly lower as compared to those without hypokalemia. Serum C-reactive protein was significantly higher in the patients with hypokalemia. Multivariate stepwise linear regression analysis revealed that the serum albumin level and the ultrafiltration volume at the peritoneal equilibration test were independent factors associated with hypokalemia. This suggests that the serum potassium level may be an important nutritional marker in CAPD patients. Further longitudinal investigation is needed to clarify this relationship.

• Hypokalemia
• Potassium
• Continuous ambulatory peritoneal dialysis
• Nutritional status

Antimicrobials are one of the most widely prescribed classes of therapeutic agents. Although adverse effects of antimicrobials are generally minimal and reversible, serious sequelae can sometimes remain, such as unusual forms of renal failure, acid base disturbance and electrolyte abnormalities. Many antimicrobials, especially vancomycin or aminoglycosides, are associated with development of acute renal failure caused by acute tubular necrosis, allergic acute interstitial nephritis, or vasculitis. Besides, some antimicrobial agents can cause serious fluid and electrolyte imbalance. To prevent these serious con-sequences, early recognition and correction of their harmful renal and electrolyte effects are required.

• Antimicrobial
• Fluid-electrolyte imbalance
• Tubular dysfunction

Inhibition of renal prostaglandin synthesis by non-steroidal anti-inflammatory drugs (NSAIDs) causes various electrolyte and acid-base disturbances including sodium retention (edema, hypertension). hyponatremia, hyperkalemia, and decreased renal function. Decreased sodium excretion can result in weight gain, peripheral edema, attenuation of the effects of antihypertensive agents, and rarely aggravation of congestive heart failure. Although rare. NSAIDs can cause hyponatremia by reducing renal free water clearance. Hyperkalemia could occur to a degree sufficient to cause cardiac arrhythmias. Renal function can decline sufficiently enough to cause acute renal failure. NSAIDs associated electrolyte and acid-base disturbances are not uncommon in some clinical situations. Adverse renal effects of NSAIDs are generally associated with prostaglandin dependent states such as volume-contracted states. low cardiac output, or other conditions that tend to compromise renal perfusion. All NSAIDs seem to share these adverse effects. In view of many NSAIDs users` susceptibility to renal adverse effects due to their underlying disease or condition, physicians should be cautious in prescribing NSAIDs to susceptible patients.

• Edema
• Hyponatremia
• Renal tubular acidosis
• Non-steroidal anti-inflammatory agents

Nephrotoxicity is the most common and clinically significant adverse effect of calcineurin inhibitors. Cyclosporine and tacrolimus nephrotoxicity is manifested by both acute azotemia and chronic progressive renal disease and tubular zdysfunction. An elevation in the plasma potassium concentration due to reduced efficiency of urinary potassium excretion is common in cyclosporine-treated patients; it may be severe and potentially life-threatening with concurrent administration of an angiotensin converting enzyme inhibitor, which diminishes aldosterone release. Tubular injury induced by cyclosporine can also impair acid excretion. This may be presented as a hyperchloremic metabolic acidosis associated with decreased aldosterone activity and suppression of ammonium excretion by hyperkalemia. Some patients treated with cyclosporine develop hypephosphatemia due to urinary phosphate wasting. Renal magnesium wasting is also common presumably due to drug effects on magnesium reabsorption. Hypomagnesemia has also been implicated as a contributor to the nephrotoxicity associated with cyclosporine. Both cyclosporine and tacrolimus are associated with hypercalciuria. Attention must be paid to drug dose, side effects, and drug interactions to minimize toxicity and maximize efficacy.

• Calcineurin inhibitors
• Acidosis
• Hyperkalemia
• Hypophosphatemia
• Hypomagnesemia
• Hypercalciuria

Hyperphosphatemia is an unusual manifestation in patients with multiple myeloma without a significantly reduced glomerular filtration rate. Serum phosphate may be falsely elevated when a large amount of paraproteins is present in the serum, because ultraviolet light absorbance is elevated with the phospho-molybdate ultraviolet assay, which is most commonly used for serum phosphate measurement. This pseudohyperphosphatemia can be confirmed by deproteinization of the serum of patients. We report a case of multiple myeloma presenting with spurious hyperphosphatemia revealing pseudohyperphosphatemia by deproteinization of serum using sulfosalicylic acid.

• Paraproteinemia
• Multiple myeloma
• Pseudohyperphosphatemia

Renal artery stenosis is a cause of secondary hypertension which can be cured by surgical or radiological intervention such as percutaneous transluminal renal artery stent placement. In this case we present a subcapsular hematoma of the kidney, a complication following percutaneous transluminal stent placement in the renal artery. Reperfusion injury to the kidney may be a possible mechanism of subcapsular hematoma of the kidney. Long standing severe renal artery stenosis and high pre- and post-procedure pressure gradient might contribute to the complication.

• Renovascular hypertension Percutaneous transluminal angioplasty
• Hematoma
• Reperfusion

Congenital adrenal hyperplasia (CAH) caused by 21-hydroxylase deficiency is an autosomal recessive disease, which leads to cortisol and aldosterone deficiency and hyperandrogenism. Typical medical treatment includes oral glucocorticoid and mineralocorticoid administration to suppress adrenal androgens and to compensate for adrenal steroid deficiencies. However, some patients stopped taking medicine without the doctor`s consent. Among these patients, four cases of CAH patients showing the presence of hyponatremia as an initial electrolyte disorder were found with adrenal adenoma. Hypersecretion of adrenocorticotrophic hormone and chronic poor compliance to therapy appears to be associated with the development of the adrenal tumor. Two cases were managed with adrenalectomy because of increasing adrenal tumor size and virilization. Whereas the other two cases did not increase in size and were observed without adrenalectomy. Therefore, it is important that patients with CAH maintain steroid medication to avoid the appearance of adrenal tumor.

• Congenital adrenal hyperplasia
• 21-hydroxylase deficiency
• Hyponatremia
• Adrenal tumor