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Clinical Observation on Hyperkalemic Distal Renal Tubular Acidosis.

Mi Jung KANG ; Choong Hwan KWAK ; Kyu Bok JIN ; Eun A WHANG ; Seung Yeup HAN ; Sung Bae PARK ; Hyun Chul KIM

Korean Journal of Nephrology.2004;23(2):263-269.

PURPOSE: Renal tubular aicdosis (RTA) is a disorder of renal acidification out of porportion to the reduction in glomerular filtration rate. Type IV RTA refers to hyperkalemic metabolic acidosis resulting from aldosterone deficiency or resistance. The incidence of each type RTA has not been reported exactly, however reports on type IV RTA have been recently increasing. METHODS: A retrospective clinical analysis was performed in 50 patients with hyperkalemic distal renal tubular acidosis diagnosed between Jan. 1984 and Feb. 2003 at Department of Internal Medicine, Keimyung University, Dongsan Medical Center. RESULTS: From 1984 to 2003, 50 cases of hyperkalemic distal renal tubular acidosis were diagnosed. The mean age was 50.8+/-19.5 years. The two most common conditions were posttransplantation (28%), and diabetes mellitus (22%), which were followed by hypertension (12%), systemic lupus erythematosus (12%), chronic renal failure (12%), and others (26%). Asymptomatic hyperkalemia (34%), and muscle weakness (28%) were the two most common clinical presentations. All patients demonstrated normal anion gap acidosis with positive urine anion gap. The mean creatinine clearance was 25.6+/-16.4 mL/min. The mean baseline PRA and aldosterone levels were 3.82+/-7.16 ng/mL/hr and 110.02+/-108.2 ng/mL, respectively. Hyperkalemia was well responded to 9-alpha-fludrocortisone, furosemide, K-exchane resin, and combinations of these regimens. CONCIUSION: Type IV RTA is the most common type of RTA in children and adults, and can be an important cause of asymptomatic hyperkalemia. Therefore, type IV RTA should be included in the diffrential diagnosis of unexplained hyperkalemia in various clinical settings.
Acid-Base Equilibrium ; Acidosis ; Acidosis, Renal Tubular* ; Adult ; Aldosterone ; Child ; Creatinine ; Diabetes Mellitus ; Diagnosis ; Furosemide ; Glomerular Filtration Rate ; Humans ; Hyperkalemia ; Hypertension ; Hypoaldosteronism ; Incidence ; Internal Medicine ; Kidney Failure, Chronic ; Lupus Erythematosus, Systemic ; Muscle Weakness ; Retrospective Studies

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Clinical Characteristics of Patients with Chronic Kidney Disease Associated with Marked Bradycardia.

Doo Hwan CHOI ; Seon Ho AHN ; Sung Won JUNG ; Yu Min LEE ; Hyun Jung KIM ; Myeung Su LEE ; Seung Hoon BAEK ; Ju Hung SONG

Korean Journal of Nephrology.2004;23(2):256-262.

Since profound hyperkalemia induces fatal arrhythmias, the recognition of its electrocardiographic manifestations is very important. The changes on the ECG correlated roughly with the severity of hyperkalemia. It has been, however, less recognized that severe hyperkalemia is associated with bradycardia. We present 14 patients with chronic kidney disease manifesting marked bradycardia in the presence or absence of hyperkalemia. It is interesting that diabetes mellitus which was complicated in 10 of 14 patients in the present study might exaggerate bradycardia with or without hyperkalemia. 9 patients, who were taking drugs such as diltiazem, beta-blocker, alpha, beta-blocker, and digoxin, developed bradycardia even when their plasma potassium concentration were moderate (<6.5 mEq/L). Therefore, we suggest that synergistic action of these drugs, hyperkalemia, diabetes mellitus, and uremic toxin in patient with chronic kidney disease might play a role in inducing bradycardia.
Arrhythmias, Cardiac ; Bradycardia* ; Diabetes Mellitus ; Digoxin ; Diltiazem ; Electrocardiography ; Humans ; Hyperkalemia ; Plasma ; Potassium ; Renal Insufficiency, Chronic*

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Clinical Characteristics and Risk Factors of Contrast Dye Nephrotoxicity in Patients Performing Arteriography.

Young Soo KIM ; Sun Wha SONG ; Young Mi KU ; Ha Hun SONG ; Sun Ae YOON ; Ho Cheol SONG ; Young Ok KIM ; Ki Tae KIM ; Yoon Sik CHANG ; Byung Kee BANG

Korean Journal of Nephrology.2004;23(2):248-255.

BACKGROUND: Because of increasing incidence of astherosclerosis, the incidence of contrast nephrotoxicity is increasing in Korea. This study was designed to investigate the clinical characteristics and risk factors of contrast dye nephrotoxcity in patients performing arteriography. METHODS: This study included 511 adult patients who performed arteriography. We retrospectively evaluated the incidence, clinical course, and risk factors of contrast dye-induced acute renal failure via medical records. Acute renal failure was defined as a rise of serum creatinine more than 50% of baseline levels 2-3 days after exposure of contrast dye. RESULTS: Of the total 511 patients, 23 patients (4.5%) had acute renal failure. The mean age of these patients was 57+/-0 years and the number of male was 14. The mean duration between the exposure and development of acute renal failure was 2.0+/-.7 days. The serum creatinine level maximally increased to 3.2+/-.9 mg/dL at 6.3+/-.1 days after the exposure. Oliguria and pulmonary edema developed in 8 and 7 patients, respectively. Four patients needed hemodialysis treatment. Of the total 23 patients with acute renal failure, 19 patients recovered with conservative treatment and 3 patients died without recovery of renal function and 1 patients progressed end stage renal failure. Renal insufficiency and dosage of contrast dye were independent risk factors of development of acute renal failure. CONCIUSION: Contrast dye-induced acute renal failure occurred in 4.5% of patients performing arteriography. Most cases of acute renal failures completely recovered but 4 case needed hemodialysis and 1 case progressed to end stage renal failure. Renal insufficiency and dosage of contrast dye were independent risk factors of development of acute renal failure.
Acute Kidney Injury ; Adult ; Angiography* ; Contrast Media ; Creatinine ; Drug-Related Side Effects and Adverse Reactions ; Humans ; Incidence ; Korea ; Male ; Medical Records ; Oliguria ; Pulmonary Edema ; Renal Dialysis ; Renal Insufficiency ; Retrospective Studies ; Risk Factors*

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Clinical Significance of Serum and Urinary Neopterin Levels in Some Renal Diseases.

Soo Suk JUNG ; Hyang KIM ; Jung Won YUN ; Jung Yel SUH ; Chan Hee JUNG ; Kyu Beck LEE

Korean Journal of Nephrology.2004;23(2):241-247.

BACKGROUND: Neopterin is a pyrazino-pyrimidine compound, produced by human monocytes or macrophages primarily upon stimulation with gamma interferon. Neopterin is a marker associated with cell- mediated immunity. The levels of neopterin in body fluids are elevated in allograft rejection, infections, autoimmune diseases, malignancies, cardiac and renal diseases. We hypothesized that the levels of serum and urine neopterin maybe elevated in some renal disease including nephrotic syndrome (NS), chronic renal failure (CRF) and end stage renal disease (ESRD). METHODS: We examnined the serum and urinary neopterin levels in 19 patients with NS underwent renal biopsy, 8 patients with CRF, 64 patients with ESRD undergoing maintenance hemodialysis. Twenty-two healthy controls were enrolled to define the normal range of neopterin levels. Serum and urinary neopterin were measured by radiommunoassay method. We also correlated the levels of serum and urinary neopterin with many clinical parameters such as WBC, hemoglobin, hematocrit, BUN, creatinine, total protein, albumin, triglyceride, iron, total iron binding capacity. RESULTS: The serum neopterin levels elevated in patients with NS (14.1+/-30.9 ng/mL), CRF (28.2+/-19.4 ng/mL) and ESRD (68.6+/-25.5 ng/mL) than control (1.6+/-0.3 ng/mL). Particularly the patients with CRF and ESRD showed statistically significant elevation (p<0.05, p<0.01). The urine neopterin levels elevated in patients with NS (203.2+/-349.6 microgramol/mol creatinine), CRF (319.2+/-107.7 microgramol/mol creatinine) and ESRD (407.9+/-256.9 microgramol/mol creatinine) than control (108.9+/-57.9 microgramol/mol creatinine). Particularly the patients with CRF and ESRD showed statistically significant elevation (p<0.05, p<0.05). The serum neopterin showed significantly positive correlation with serum creatinine levels, inverse correlation with total iron binding capacity and serum triglyceride levels among clinical parameters in all groups (respectively p<0.01). The urine neopterin showed significant inverse correlation with hemoglobin (p< 0.05). CONCIUSION: The serum and urinary neopterin levels elevated in patients with some renal diseases. And also neopterin levels showed clinical correlations with some renal parameters in these patients. We suggest that serum and urinary neopterin levels may be useful marker to predict disease acitivity and prognosis in some renal diseases. They should be confirmed by a prospective study during a long-lasting and in a higher number of patients.
Allografts ; Autoimmune Diseases ; Biopsy ; Body Fluids ; Creatinine ; Hematocrit ; Humans ; Interferons ; Iron ; Kidney Failure, Chronic ; Macrophages ; Monocytes ; Neopterin* ; Nephrotic Syndrome ; Prognosis ; Reference Values ; Renal Dialysis ; Renal Insufficiency, Chronic ; Triglycerides

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Effect of Losartan Treatment on Proteinuria and Urinary Transforming Growth Factor-beta1 in Human Chronic Glomerulonephritis.

Hyeong Cheon PARK ; Beom Seok KIM ; Hoon Young CHOI ; Shin Wook KANG ; Kyu Hun CHOI ; Sung Kyu HA ; Ho Yung LEE ; Dae Suk HAN

Korean Journal of Nephrology.2004;23(2):231-240.

BACKGROUND: Urinary TGF-beta1 reflects intrarenal TGF-beta1 production and is increased in patients with progressive nephropathies. We studied the effects of angiotensin receptor blocker (ARB) on serum and urinary TGF-beta1 excretion in chronic glomerulonephritis patients with proteinuria. Also the role of urinary TGF-beta1 in ARB induced antiproteinuric responses was evaluated. METHODS: Patients with non-diabetic chronic renal disease with proteinuria of 1 g or more were enrolled in this open, prospective study. After four weeks of washout period, the patients received losartan 50 mg daily followed by 100 mg in two treatment periods each lasting 12 weeks. Clinical parameters and urinary indices including proteinuria and urinary TGF-beta1 were measured at baseline and after each 12 week treatment period. RESULTS: Among the 42 patients who completed the study, 31 responded to ARB therapy determined as a decrease in proteinuria by 30% (responders), and 11 did not respond (non-responders). ARB treatment controlled blood pressure to a similar degree in both responders and non-responders. Renal function and other biochemical parameters did not change during the study period. Both doses of losartan significantly lowered proteinuria and urinary TGF-beta1 excretion in responders (50 mg: 33.4% and 29.0%, 100 mg: 64.1% and 45.8%, respectively, p<0.05). In contrast, non-responders showed no significant reduction in proteinuria and no further decrease in urinary TGF-beta1 after 100 mg treatment. Urinary TGF-beta1 excretion lacked any correlation between clinical parameters such as proteinuria or renal function. Responders were younger, showed lower baseline proteinuria and urinary TGF-beta1 excretion and greater reduction in urinary TGF-beta1 excretion after ARB treatment. However, lower baseline urinary TGF-beta1 excretion was the only significant predictor of response to ARB therapy. CONCIUSION: Our data suggest that ARB therapy in nondiabetic proteinuric chronic glomerulonephritis patients reduces proteinuria and urinary TGF-beta1 excretion and baseline urinary TGF-beta1 excretion may predict antiproteinuric response to ARB therapy.
Angiotensins ; Blood Pressure ; Glomerulonephritis* ; Humans* ; Losartan* ; Prospective Studies ; Proteinuria* ; Renal Insufficiency, Chronic ; Transforming Growth Factor beta1

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Estimation of GFR Using Iohexol Plasma Clearance in Korean without Renal Disease.

Woo Heon KANG ; Tae Geun KWON ; Dae Joong KIM ; Myoung Jae KANG ; Hyeon Jung BAEK ; Ho Myoung YEO ; Young Hwan LIM ; Jung Ah KIM ; Bang Hoon LEE ; Beom KIM ; Kyu Beck LEE ; Wooseoung HUH ; Yoon Gu KIM ; Ha Young OH

Korean Journal of Nephrology.2004;23(2):223-230.

BACKGROUND: Plasma clearance of iohexol (Omnipaque(r)) which used widely in radiologic procedure is considered as useful method for estimation of GFR because iohexol is neither reabsorbed nor secreted from tubule after filtered as inulin and its extrarenal clearance is negligible. Plasma clearance of iohexol can be calculated from two compartment model or one compartment model with Brochner-Mortensen (B-M) modification which convenient and reliable. But there were controversies about sufficient sampling numbers and times for B-M modification of iohexol clearance. METHODS: Nineteen healthy Korean without renal disease underwent measurement of iohexol clearance. Iohexol was given as a single iv dose, and 14 blood sample were drawn up to 300 min. A reference GFR was iohexol clearance calculated from two-compartment model using 14 samples (CL-T). From 8, 3 and 2 samples clearances were calculated by B-M modification (CL-M8, 3 and 2 respectively). The accuracy of estimates was evaluated as percent of estimates falling within 10% above or below the reference GFR. Accuracy of CCr and equations for GFR estimation were also compared. RESULTS: CL-T, CL-M8, CL-M3 and CL-M2 were not different (101.9+/-24.0, 101.9+/-18.7, 101.7+/-18.6, 101.9+/-19.5 mL/min/1.73 m2 respectively). Accuracy of CL-M8, 3 and 2 were not different (74%, 84% and 79% respectively, p>0.05). MDRD equation had higher accuracy (47%) compared with other equations. CONCIUSION: These results indicate that sampling number for measuring iohexol plasma clearance using simplified method might be reduced to only two without accuracy loss in Korean without renal disease.
Inulin ; Iohexol* ; Plasma*

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Characteristics of Bromate-induced Acute Renal Failure in Rats.

Seok Joon SHIN ; Ho Seon PARK ; Young Jin CHOI ; Chul Woo YANG ; Dong Chan JIN ; Yong Soo KIM ; Jin KIM ; Yoon Sik CHANG ; Byung Kee BANG

Korean Journal of Nephrology.2004;23(2):213-222.

BACKGROUND: Bromate has been reported to cause hemolytic anemia, acute renal failure, hearing and visual impairments. Several mechanisms for bromate-induced renal damage have been suggested including direct tubular toxicity due to induction of active oxygen radicals. However, the mechanism has not been clearly determined. The purpose of this study was to analyze the clinical characteristics of acute renal failure and renal tissue injuries following bromate intoxication. METHODS: Sprague-Dawley rats were intraperitoneally treated with potassium bromate 75 mg/kg (B75) or 150 mg/kg (B150). Blood urea nitrogen, serum creatinine, 24 hours urine volume, and creatinine clearance rate were measured at 24 hours, 48 hours, 1 week and 2 weeks after bromate injection. Light microscopic findings and the expressions of Na+ - K+ - ATPase-alpha 1 and aquaporin-2 in renal tissues were examined by PAS stain and immunohistochemical stain. RESULTS: Potassium bromate induced acute renal failure. In B75, acute renal failure was recovered after 1 week. However, in B150, all rats were dead in 48 hours due to severe uremia. Light microscopic examination revealed severe acute tubular necrosis in B75 and B150, which was severer in B150 compared to B75, and was more prominent in the tubules of the inner strip of outer medulla compared to cortex. Na+ - K+ - ATPase-alpha 1 expression was not changed in the renal cortex after bromate treatment. However, the expression was slightly decreased in the inner strip of outer medulla at 48 hours and recovered at 2 weeks in B75, and it was severely decreased at 24 and 48 hours in B150. The expression of aquaporin-2 in the inner strip of outer medulla was increased in B75 and was decreased in B150. CONCIUSION: Bromate induced acute tubular necrosis in inner strip of outer medulla of the kidney. Low dose bromate induced the decreased expressions of Na+ - K+ - ATPase-alpha 1, which lead to polyuric acute renal failure, but high dose bromate induced severe acute tubular necrosis, which lead to severe oliguric acute renal failure.
Acute Kidney Injury* ; Anemia, Hemolytic ; Animals ; Aquaporin 2 ; Blood Urea Nitrogen ; Creatinine ; Hearing ; Kidney ; Necrosis ; Potassium ; Rats* ; Rats, Sprague-Dawley ; Reactive Oxygen Species ; Uremia ; Vision Disorders

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Protective Effect of Melatonin on the Nephrotoxicity by Cisplatin.

Hye Jung CHOI ; Young Ho SHIN ; Kyo Cheol MUN ; Dae Kyu SONG ; In Cheol KIM ; Sang Hyuck SEO ; Chun Sik KWAK ; Eun Ju CHANG ; Hyun Chul KIM

Korean Journal of Nephrology.2004;23(2):205-212.

BACKGROUND: Cisplatin (CP), an antitumor agent widely used in the treatment of cancers, has nephrotoxicity. This side effect is closely related to oxidative stress. In the present study, we attempted to reduce CP-induced nephrotoxicity in rats by administering melatonin, an antioxidant. METHODS: Male Sprague-Dawley rats were divided into different groups and were treated as follows: (1) saline control; (2) CP (16 mg/kg, i.p.); (3) CP plus melatonin (10 mg/kg, i.p.). The rats were sacrificed at the 6th day after CP treatment. To evaluate renal damage, BUN, serum creatinine, creatinine clearance and microscopic examination were done. Hydrogen peroxide which is one of the oxygen free radicals, and malondialdehyde which is known as a marker of the oxygen free radical mediated injury, and the activities of the antioxidant enzymes such as superoxied dismutase, catalase, and glutathione peroxidase were also measured. RESULTS: CP-treated rats showed the increase of BUN, serum creatinine, malondialdehyde, hydrogen peroxide and superoxide dismutase (SOD) in kidney. And CP-treated rats also showed the decrease of creatinine clearance and catalase levels. CP-treated rats showed severe tubular necrosis in proximal convoluted tubules under the light microscopic examination. The light microscopic finding and all of the parameters except SOD were restored in the rats injected with CP plus melatonin than those with CP alone. SOD level was higher in the rats injected with CP plus melatonin than that with CP alone. CONCIUSION: These results suggest that melatonin suppresses CP-induced nephrotoxicity by suppressing the production of reactive oxygen species via the activation of SOD and catalase.
Animals ; Catalase ; Cisplatin* ; Creatinine ; Free Radicals ; Glutathione Peroxidase ; Humans ; Hydrogen Peroxide ; Kidney ; Male ; Malondialdehyde ; Melatonin* ; Necrosis ; Oxidative Stress ; Oxygen ; Rats ; Rats, Sprague-Dawley ; Reactive Oxygen Species ; Superoxide Dismutase

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Effect of Cyclosporine Withdrawal on Apoptotic Cell Death in a Model of Chronic Cyclosporine Nephrotoxicity.

Bum Soon CHOI ; Hyung Wook KIM ; Hye Eun YOON ; Ji Hyun KIM ; Bo Kyung SUN ; Sun Woo IM ; Chan LEE ; Chul Woo YANG ; Yong Soo KIM ; Euy Jin CHOI ; Yoon Sik CHANG ; Byung Kee BANG

Korean Journal of Nephrology.2004;23(2):195-204.

BACKGROUND: Cyclosporine (CsA) used in a dual or triple regimen is the current primary immunosuppressant for prevention of renal allograft rejection. Although the introduction of CsA into clinical practice has resulted in a 10 to 15% increase of the 1-year graft survival rate, little has been gained to improve long-term graft survival. Long-term administration of CsA causes a progressive renal failure, a renal striped interstitial fibrosis, a tubular atrophy, and a hyalinosis of the afferent arteriole. Previous studies have shown that apoptotic cell death is increased in CsA-treated kidneys and plays a role in interstitial fibrosis. This study evaluates the effect of CsA withdrawal on CsA nephrotoxicity. METHODS: Sprague-Dawley rats on low-salt diet had been treated with CsA (7.5 mg/kg/day) for five weeks and then CsA had been withdrawn for the next five weeks. The weights, systolic blood pressure, plasma CsA concentration, renal function (serum creatinine, creatinine clearance) and histologic parameter (arteriolopathy, interstitial fibrosis) of the rats were compared. Apoptotic cell death was detected by TUNEL assay. RESULTS: CsA-treated rats showed decreased renal function compared with vehicle (VH) group. With CsA withdrawal, renal function was significantly improved compared with the CsA-treated rats. CsA-treated rats showed increased arteriolopathy and interstitial fibrosis compared with VH group. With CsA withdrawal, renal histology was significantly improved. CsA-treated rats showed increased TUNEL-positive cell compared with VH group. With CsA withdrawal, apoptotic cell death was decreased. Using bivariate correlation analysis, CsA induced apoptotic cell death correlated with arteriolopathy and interstitial fibrosis. CONCIUSION: CsA withdrawal in CsA nephrotoxicity decreased apoptotic cell death and improved renal function and renal histiology. This finding provides a rationale for CsA withdrawal in CsA nephrotoxicity. Further investigation should be directed to explore the effects of the accumulated CsA dose and the timing of CsA withdrawal for regression CsA nephrotoxicity.
Allografts ; Animals ; Apoptosis ; Arterioles ; Atrophy ; Blood Pressure ; Cell Death* ; Creatinine ; Cyclosporine* ; Diet, Sodium-Restricted ; Fibrosis ; Graft Survival ; In Situ Nick-End Labeling ; Kidney ; Plasma ; Rats ; Rats, Sprague-Dawley ; Renal Insufficiency ; Weights and Measures

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Quantification of Endothelin-1 mRNA and Endothelin Receptor B mRNA from Cortex and Inner Medulla of Mouse Kidney Using Real-time RT-PCR.

Do Whan AHN

Korean Journal of Nephrology.2004;23(2):188-194.

BACKGROUND: Endothelin-1 (ET-1) production and ET receptor type B (ETRB) density in the kidney increase along the corticomedullary axis. Northern blot showed that preproET-1 mRNA message was higher in medulla than cortex. ETRB mRNA expression by nested RT-PCR was similar to that of ET-1 mRNA. This study was undertaken to evaluate the renal expression pattern of ET-1 and ETRB mRNAs by Northern blot and nested RT-PCR using a real-time RT-PCR technique. METHODS: The cortex and inner medulla of mouse kidney were dissected out and real-time RT- PCR was performed. Fluorescent ntensity of PCR was recorded using the DNA-intercalating dye SYBR green. Melting curve analysis was utilized for selection of sequence-specific PCR products. For the comparision of relative expression of mRNA in the cortex and inner medulla, Pfaffl's formula (Pfaffl MW: Nucleic Acids Res 29: 2003-2007, 2001) was used. RESULTS: Peak Tms of amplified beta-actin, ET-1 and ETRB genes from inner medulla were 88.2degrees C, 90.5degrees C and 85.5degrees C, respectively. In the cortex, expression of ETRB mRNA was greater on an average by 4.59 cycles (24.59=24 times more abundant) compared to that of ET-1 mRNA. In the inner medulla, ETRB message was 25 times greater than ET-1 message. When ET-1 mRNA expression was compared between cortex and inner medulla the ratio was 3.2, indicating that inner medulla contained three times more ET-1 mRNA than cortex. The expression ratio of cortex to inner medulla of ETRB mRNA was 3.3. CONCLUSION: These results suggest that ET-1 mRNA and ETRB mRNA are more abundantly expressed in medulla than cortex and that the distribution of these mRNAs may be intimately related to that of their respective gene products.
Actins ; Animals ; Axis, Cervical Vertebra ; Blotting, Northern ; Endothelin-1* ; Endothelins* ; Freezing ; Kidney* ; Mice* ; Nucleic Acids ; Polymerase Chain Reaction ; Receptors, Endothelin* ; RNA, Messenger*

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