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Abstract

K. Yokoyama, T. Shigematsu, T. Tsukada, S. Hara, A. Yamada, Y. Kawaguchi and T. Hosoya

¹The Division of Nephrology and Hypertension, Jikei University School of Medicine, Tokyo, ²Nephrology and Dialysis Unit, Department of Internal Medicine, Sakura National Hospital, Chiba, ³Department of Clinical Physiology, Toranomon Hospital, Tokyo, ⁴Kidney Center, Toranomon Hospital, Tokyo, Japan
Aim: The basic mechanism of secondary hyperparathyroidism is still unclear, but a change in Ca2+ sensing by parathyroid cells is possibly involved in this uremic complication. A rightward shift of the calcium set-point and an increase of the minimum secretion rate have been found in secondary hyperparathyroidism, indicating abnormal calcium sensing. Methods: We evaluated the effect of calcium sensing receptor (CaR) gene polymorphism (codon G990R) on the response of the parathyroid gland to moderate hypercalcemic suppression in 77 ESRD patients on regular hemodialysis (HD using 2.5 mEq/l Ca2+ dialysate). All patients underwent an HD session with 3.0 mEq/l Ca2+ dialysate to suppress parathyroid hormone (PTH). Then we investigated the effect of CaR gene polymorphism on the parathyroid response to hypercalcemic stimulation. Results: Patients were divided into 3 groups on the basis of genotype (GG = 33 patients (42.9%), GR = 39 patients (50.6%), RR = 5 patients (6.5%)). Baseline intact PTH levels in patients without the R allele were not significantly different from those in patients with the R allele (GG group, 181.4 ± 31.1 pg/ml vs. GR and RR groups, 230 ± 51.2 pg/ml: mean ± SEM). The significant effect of moderate hypercalcemic suppression on the intact PTH level was observed in the GG group (p < 0.01) but not in the GR and RR groups, despite the identical increase in Ca2+. Conclusion: Our results suggest that CaR gene polymorphism (codon G990R) influences the responsiveness of the parathyroid gland to changes of extracellular Ca2+ in ESRD patients. The glands of patients with the GG genotype of the CaR gene may be more sensitive to extracellular Ca2+ changes.

Abstract

M. Numata, M. Nakayama, T. Hosoya, C.M. Hoff, C.J. Holmes, M. Schalling, L. Nordfors and B. Lindholm

¹Division of Kidney and Hypertension, Department of Internal Medicine, Jikei University School of Medicine, Tokyo, Japan, ²Baxter Healthcare Renal Division Scientific Affairs, Baxter Healthcare Corporation, McGaw Park, IL, USA, ³Department of Molecular Medicine, Karolinska Institutet, Stockholm, and ⁴Department of Clinical Science, Divisions of Renal Medicine and Baxter Novum, Huddinge University Hospital, Huddinge, Sweden
Encapsulating peritoneal sclerosis (EPS) is a serious complication of PD. The cause(s) of EPS are unknown but may include peritonitis and long duration of PD treatment. However, EPS may also develop in some patients without a history of peritonitis or with rather short duration of PD therapy. It has been suggested that an increasing peritoneal solute transport rate (PSTR) as a function of time on PD treatment is a risk factor for EPS development after transfer to hemodialysis, and that high PSTR is associated with an increased peritoneal microvessels surface area. Other putative mechanisms might include advanced glycated end products (AGE) and their receptors, RAGE. The purpose of this study was to investigate genetic variations in PD patients developing EPS in comparison to PD patients without EPS. SNPs in genes related to angiogenesis as well as RAGE were analyzed. Twenty patients (M/F: 12/8, mean age at start of PD 42.2 years, mean duration of PD 8.4 years) who were diagnosed as EPS during the period 1982 – 2002 at Jikei University Hospital and a matched control group (n = 20) of nonEPS PD patients were studied. The following 5 SNPs were analyzed: VEGF 936 C/T, ecNOS –786 T/C, 298 Glu/Asp, and RAGE –374 T/A, and –429 T/C. The SNPs were analyzed by the pyrosequencing method. The C allele (T/C and C/C) in the RAGE –429T/C genotype was not found in any of the EPS patients (EPS, T/T: 20/20 (100%), nonEPS, T/T: 15/20 (75%), T/C: 4/20 (20%), C/C: 1/2 0(5%), nonC allele vs C allele, p = 0.013), although every allele was found in other SNPs. We conclude that these preliminary data show that whereas genotypes directly related to angiogenesis did not differ between EPS and nonEPS patients, it is noteworthy that no patients in the EPS group had a C allele in the RAGE –429T/C genotype. This might indicate a possible genetic contribution to the development of EPS that is related to RAGE.Correspondence to:
Dr. M. Numata
Division of Kidney and Hypertension
Department of Internal Medicine
Jikei University School of Medicine
3-19-18, Nishishinbashi
Minato-ku, Tokyo, 105-8471, Japan
Email: [email protected]

Abstract

M. Nakayama¹, H. Nakano²,³, N. Tsuboi³, T. Kurosawa⁴, Y. Tsuruta⁵, Y. Iwasaki⁶, K. Yokoyama³, T. Hosoya³ and M. Fukagawa⁷

¹Research Division of Dialysis and Chronic Kidney Disease, Tohoku University Graduate School of Medicine, Sendai, ²Dialysis Center, Kashima Hospital, Iwaki, ³Department of Kidney and Hypertension, The Jikei University School of Medicine, Tokyo, ⁴Dialysis Division, Sumiyoshi Clinic Hospital, Mito, ⁵Dialysis Division, Meiyo Clinic, Toyohashi, Aichi, ⁶Nursing and Health Science, Oita University of Nursing and Health Sciences, Oita, ⁷Division of Nephrology and Dialysis Center, Kobe University School of Medicine, Kobe, Japan
Objective: It is revealed that LVH is one of risk factors for the development of cardiac complications in long-term HD patients. Therefore, maneuvers to reduce hypertrophy of cardium are very important for improving life prognosis. Angiotensin II receptor blockade (ARB) could reduce LVH in general populations without renal failure. However, no conclusive data has been available regarding the clinical consequences of ARB administration on the regression of LVH in HD patients. Furthermore, it has not clearly determined if ACE gene polymorphism has a possible influential effect on it. This study is conducted to clarify these issues. Subjects and method: 32 hypertensive patients on regular HD (male/female: 21/11, mean age: 60.5 years, mean duration of HD: 52.8 months) were studied. Patients were classified into two groups according to the different type of ACE gene polymorphism: cases with D allele (DD/ID; D group: n = 13) and those without (II; non-D group: n = 19). All patients were administered ARB (losartan 50 – 100 mg/day) and echocardiography (UCG) was performed at 6-month-interval regularly until the end of observation (24 months). Results: Before the commencement of ARB, no differences were found between the two groups, neither in mean blood pressure (MBP: D group/non-D group: 120 ± 13 vs. 115 ± 14 mmHg) nor in left ventricular mass index (LVMI: D/non-D: 172 ± 41 vs. 165 ± 41 g/m2). During the 24-month follow-up, there were significant and similar reductions in MBP in both groups. In respect to LVMI, a significant reduction of LVMI was found in the D group after six months (p < 0.01 vs. basal) with a final reduction rate (FRR) –26 ± 13%, whereas in the non-D group it was found at 24 months (p < 0.01 vs. basal) with FRR –11 ± 16% (p < 0.01 vs. D group). There were significant differences between the two groups at all points (p < 0.05 at 6, 18 and 24 months, p < 0.005 at 12 months, respectively). Conclusion: It is indicated that ARB could insert a regression effect on LVH predominantly in patients with D allele ACE polymorphism, due partly to factor (s) independent of its anti-hypertensive effect.Correspondence to:
M. Nakayama, MD
Research Division of Dialysis and Chronic Kidney Disease
Tohoku University Graduate School of Medicine
Seiryo machi 1-1 Aoba-ku
Sendai, 980-8574, Japan
Email: [email protected]

Abstract

K. Yokoyama, H. Yoshida, N. Matsuo, Y. Maruyama, Y. Kawamura, R. Yamamoto, K. Hanaoka, M. Ikeda, H. Yamamoto, M. Nakayama, Y. Kawaguchi and T. Hosoya

¹Division of Kidney and Hypertension, Department of Internal Medicine,
Jikei University School of Medicine, Tokyo and ²Research Division of Dialysis and Chronic Kidney Disease, Tohoku University Graduate School of Medicine, Sendai Miyagi, Japan
Background: Encapsulating peritoneal sclerosis (EPS) is a serious complication in patients undergoing continuous ambulatory peritoneal dialysis (CAPD) or automated peritoneal dialysis (APD). The aim of this study was to find a predictor for EPS. Methods: Patients with EPS who were detected by a historical cohort study using clinical data of 219 CAPD patients at our hospital. We recruited 25 patients with EPS who were compared with the patients without EPS who were matched for age and dialysis period as controls. Differences between the two groups (non-EPS group and EPS group) with respect to age, gender, primary disease, dialysis period, serum urea nitrogen, serum creatinine, β₂MG, CRP and PET (peritoneal equilibration test) category (determined by the peritoneal function testing) were analyzed. Results: According to multiple regression analysis, a high β₂MG level was an independent risk factor for EPS (odds ratio 1.162, 95% confidence interval 1.026 – 1.317, p = 0.018). Other clinical markers did not show positive significance. A ROC (receiver operating characteristic) curve was prepared to evaluate the suitability of β₂MG measurement as a screening test. The sensitivity was 64% and the specificity was 80% when a β₂MG level of 37.0 mg/dl was taken as the cut-off value. The odds ratio for occurrence of EPS was 8.8 when β₂MG level was in the range of 35 – 40 mg/dl, 13.5 when β₂MG level was > 40 mg/dl and 1 when β₂MG level was < 30 mg/dl. Conclusion: These findings suggest that β₂MG is useful as a screening test for the onset of EPS, and that β₂MG and accumulation of middle-molecular uremic substances may be related to the pathophysiology of EPS.Correspondence to:
K. Yokoyama, MD, Division of Kidney and Hypertension, Department of Internal Medicine, The Jikei University School of Medicine, Tokyo, Japan
Email: [email protected]

Abstract

S. Kagami¹, I. Ohkido¹, K. Yokoyama¹, T. Shigematsu² and T. Hosoya¹

¹Department of Internal Medicine, Division of Nephrology and Hypertension, The Jikei University School of Medicine, Tokyo, ²Department of Internal Medicine, Division of Nephrology and Blood Purification Medicine, Wakayama Medical University, Wakayama, Japan
Background: Both fibroblast growth factor-23 (FGF-23) and osteoprotegerin (OPG) are associated with phosphate metabolism, and are produced by bone tissue. Methods: In order to clarify the influence of bone turnover on phosphate metabolism, we examined the response of FGF-23 to an oral phosphate load in 4 groups of mice (2 OPG knockout (KO) and 2 wild-type (WT) groups) given either a high-phosphate diet or a normal diet by performing serum and urinary biochemical assays. Results: Although there was no significant difference in serum phosphate/ calcium levels between the groups, the decrease in tubular reabsorption rate of phosphate (%TRP) by oral phosphate load was smaller in the OPG KO mice than in the WT mice. FGF-23 level was significantly increased by a high-phosphate diet in WT mice, but not in OPG KO mice. However, there was no significant difference of intact PTH and calcitriol levels between the OPG KO and WT mice. Conclusion: Therefore, OPG may play a key role in mediating the response of FGF-23 to an oral phosphate load in bone cells.Correspondence to:
S. Kagami, MD; Division of Nephrology and Hypertension, Department of Internal Medicine,
The Jikei University School of Medicine, 3-25-8, Nishi-shimbashi, Minato-ku, Tokyo, 105-8461, Japan
Email: [email protected]

Abstract

H. Kobayashi¹, G. Tokudome¹, Y. Hara¹, N. Sugano¹, S. Endo¹, Y. Suetsugu¹, S. Kuriyama² and T. Hosoya¹

¹Hypertension Research Unit, Division of Nephrology and Hypertension, Department of Internal Medicine, Jikei University School of Medicine, and ²Division of Nephrology, Saiseikai Central Hospital, Tokyo, Japan
Objective: Insulin resistance may contribute to the pathogenesis of hypertension and progressive chronic kidney disease (CKD), however, few clinical studies have explored the role of insulin resistance in predicting the deterioration of renal function in CKD patients. Materials and methods: Enrolled in the study were non-diabetic hypertensive patients with CKD Stage 3. Insulin resistance was assessed by a homeostasis model assessment of insulin resistance (HOMA-R) measured at the entry to the study. Patients were followed for 3 years and comparisons of renal and metabolic parameters were made in conjunction with HOMA-R between entry and the end of the study period. The insulin-resistant (IR) group was defined as patients with HOMA-R 2.0 and more, and the insulin-sensitive (IS) group as those with HOMA-R < 2.0. Results: Blood pressure in both groups was equally controlled below 130/80 mmHg throughout the observation period. The degree of insulin resistance HOMA-R and immunoreactive insulin (IRI) remained unchanged in the IS group, however, both were ameliorated in the IR group (HOMA-R, from 3.4 ± 1.5 – 3.0 ± 1.1, p = 0.022 and IRI, from 14.4 ± 6.1 µU/ml – 12.6 ± 6.8 µU/ml, p = 0.012). Creatinine clearance (CCr) and estimated glomerular filtration rate (e-GFR) decreased and serum creatinine (Cr) concentration increased in all patients. The decline in CCr calculated as the slope of the reciprocal of serum Cr concentration (1/Cr) was greater in the IR group (0.007 ± 0.004 (1/Cr/dl/mg/month) than in the IS group (0.003 ± 0.002 (1/Cr/dl/mg/month), p < 0.001). Linear regression analysis showed that the slope of 1/Cr was negatively correlated with HOMA-R, IRI, BMI, respectively. Furthermore, stepwise regression analysis showed that the independent variables to explain the decline in renal function were HOMA-R and IRI. Conclusion: Insulin resistance is a significant risk factor for the deterioration of renal function in hypertensive non-diabetic patients with CKD.Correspondence to:
S. Kuriyama, MD
Division of Nephrology
Saiseikai Central Hospital
1-4-17, Mita, Minato-ku, Tokyo, Japan
Email: [email protected]

Abstract

T. Suzuki, Y. Miyazaki, A. Shimizu, Y. Ito, H. Okonogi, M. Ogura, Y. Utsunomiya, T. Kawamura and T. Hosoya

Division of Kidney and Hypertension, Department of Internal Medicine, Jikei University School of Medicine, Nishishinbashi, Minato-ku, Tokyo, Japan
Aims: Inhibition of the renin-angiotensin system (RAS) decreases proteinuria in IgA nephropathy and often retards disease progression. However, its antiproteinuric efficacy varies considerably among patients or different stages in a single patient. We sought for the factor(s) underlying the variation in urinary protein excretion in RAS inhibitor-treated outpatients with IgA nephropathy. Patients: 43 patients with biopsy-proven IgA nephropathy, moderate proteinuria (0.5 – 3.5 g/day), normal to moderately-low estimated GFR (eGFR) (28.6 – 114.2 ml/min/1.73 m2) and normal blood pressure, prehypertension or mild hypertension (systolic/diastolic blood pressures < 160/100 mmHg) were placed on RAS inhibitors following diagnosis. Method: Excretion of urinary protein (UprV) and sodium (UNaV), estimated protein intake (EPI) and the mean blood pressure (MBP) were determined on 12 consecutive visits for an average duration of 17.6 months. Analyses were performed to determine which factor(s) influenced the variation in UprV. Results: 14 patients (32.6%) showed a significant correlation between UprV and UNaV, whereas UprV correlated significantly with EPI or MBP in 7 (16.3%) and 3 patients (7.0%), respectively. The 14 patients were characterized by lower eGFR and more extensive glomerulosclerosis and tubulointerstitial damage at baseline than the other 29 patients. The UprV-UNaV correlation was significant in 8 of 12 patients (66.7%) with eGFR < 60 ml/min/1.73 m² and in 6 of 29 patients (19.4%) with eGFR >= 60 ml/min/1.73 m² (p < 0.05). The UprV/UNaV regression lines were significantly steeper with more extensive glomerulosclerosis (p < 0.05) and tubulointerstitial damage (p < 0.05) at baseline. The lines also tended to be steeper with lower baseline eGFR (p = 0.062). Conclusions: These results showed that the antiproteinuric effect of RAS inhibitors becomes susceptible to an increase in urinary sodium excretion as renal function and functioning nephron mass decline with the progression of renal histological damage. Stringent dietary sodium restriction is required to maximize the antiproteinuric effect of RAS inhibitors in outpatients with IgA nephropathy.Correspondence to:
Y. Miyazaki, MD, PhD
Division of Kidney and Hypertension
Department of Internal Medicine
Jikei University School of Medicine
3-25-8, Nishishinbashi, Minato-ku
Tokyo, 105-8461 Japan
Email: [email protected]

Abstract

Clinical Nephrology, Vol. 74 – No. 3/2010 (209-216)

Clinical impact of a combined therapy of peritoneal dialysis and hemodialysis

N. Matsuo¹, K. Yokoyama¹, Y. Maruyama¹, Y. Ueda¹, H. Yoshida¹, Y. Tanno¹, R. Yamamoto¹, H. Terawaki¹, M. Ikeda¹, K. Hanaoka¹, H. Yamamoto¹, M. Ogura¹, S. Watanabe², Y. Kimura¹ and T. Hosoya¹

¹Division of Kidney and Hypertension, Department of Internal Medicine, The Jikei University School of Medicine, Tokyo, and ²Department of Internal Medicine, Kobari General Hospital, Chiba, Japan
Aims: Although peritoneal dialysis (PD) is recommended as the first-line treatment for end-stage renal disease, limitations exist to achieving good clinical status when the residual renal function (RRF) has declined. Combined therapy with PD and hemodialysis (HD) is the treatment of choice for patients who cannot control body fluid status and/or cannot obtain adequate solute removal by PD alone. The aim of this study was to evaluate the clinical efficacy of this combined therapy. Methods: In this retrospective study, 53 patients on PD and diagnosed with underdialysis and/or overhydration with declining RRF were recruited. Parameters of volume control, uremic solute removal, anemia, and predictors for encapsulating peritoneal sclerosis (EPS) were compared before and 1 year after combined therapy. Results: The patients’ hydration status improved significantly with reductions in atrial natriuretic peptide and blood pressure. Serum creatinine and beta2 microglobulin also decreased significantly. The hemoglobin level increased remarkably from 8.2 ± 1.6 to 10.7 ± 1.2 g/dl (p < 0.01) and the reticulocyte count also increased significantly, even though at the same time the dose of recombinant human erythropoietin decreased significantly. The dialysate to plasma creatinine ratio obtained from the fast peritoneal equilibration test (PET) decreased significantly from 0.65 ± 0.11 to 0.59 ± 0.13, and the level of interleukin 6 in PET drainage also significantly decreased. Furthermore, serum C-reactive protein and fibrinogen decreased significantly. Conclusions: Combined therapy with PD and HD is an effective way to control fluid status and to correct inadequate solute removal, leading to improvement in inflammation, peritoneal function and anemia.Correspondence to:
Dr. N. Matsuo
Division of Kidney and Hypertension
Department of Internal Medicine
The Jikei University School of Medicine
3-25-8 Nishi-shimbashi Minato-ku
Tokyo 105-8461, Japan
Email: [email protected]

Abstract

Clinical Nephrology, Vol. 75 – No. 1/2011 (1-7)

Difference in coronary artery intima and media calcification in autopsied patients with chronic kidney disease

H. Yoshida¹, K. Yokoyama¹, T. Yaginuma¹, I. Ohkido¹, H. Yamamoto¹, Y. Utsunomiya¹, M. Kawakami² and T. Hosoya¹

¹Division of Kidney and Hypertension, Department of Internal Medicine, The Jikei University School of Medicine, Tokyo, and ²Department of Pathology, Seirei Sakura Citizen Hospital, Sakura, Japan
Background: In patients with chronic kidney disease (CKD), coronary artery calcification occurs at two distinct sites in the vessel wall: the intima and the media. Arterial media calcification (AMC), a nonocclusive condition, affects hemodynamics differently compared to arterial intima calcification (AIC), which occurs in atherosclerotic plaques. Arterial calcification is considered a cell-regulated process resembling intramembranous bone formation. The purpose of this retrospective observational study was to clarify the morphological differences between AIC and AMC and to evaluate the role of vascular smooth muscle cells (VSMCs) and macrophages in AIC and AMC formation. Methods: We histologically analyzed 14 tissue specimens from 14 autopsies of patients with CKD Stage 5D who underwent hemodialysis and 5 specimens from 5 patients with CKD Stage 2 – 3 (90 ml/min/1.73 m² > estimated GFR >= 30 ml/min/1.73 m²). We performed immunohistochemical staining of osteopontin (OPN) as a marker for bone matrix protein, alpha-smooth muscle actin (alphaSMA) for VSMCs, Cbfa1/Runx2 as a marker for osteoblastic differentiation of VSMCs, and CD68 for macrophages. Results: In the CKD 2/3 group, we also found AIC and AMC. OPN and CD68 expression in the CKD 2/3 group was similar to that in the CKD 5D group. Although we did not find Cbfa1/Runx2 positive cell expression in the CKD 2/3 group, we did find it in the CKD 5D group. We found CD68-positive cells predominantly in AIC and absent in AMC in both groups. Conclusions: These findings suggest that the influence of Cbfa1/Runx2 pathway in coronary artery calcification depends on the CKD Stage. Expression of CD68-positive cells depends on the location of the coronary artery calcification.Correspondence to:
H. Yoshida, MD
Division of Kidney and Hypertension
Department of Internal Medicine
The Jikei University School of Medicine
3-25-8, Nishi-Shinbashi, Minato-ku
Tokyo, 105-8471, Japan
Email: [email protected]

Abstract

International Journal of Clinical Pharmacology and Therapeutics, Vol. 48 – No. 11/2010 (751-755)

Effects of probenecid on the pharmacokinetics of mizoribine and co-administration of the two drugs in patients with nephrotic syndrome

Y. Utsunomiya¹, Y. Hara¹, H. Ito¹, H. Okonogi¹, Y. Miyazaki¹, Y. Hashimoto² and T. Hosoya¹

¹Division of Kidney and Hypertension, Department of Internal Medicine, The Jikei University School of Medicine, Tokyo, and ²Graduate School of Medicine and Pharmaceutical Sciences, University of Toyama, Toyama, Japan
Probenecid (PRB) is an agent that reduces the systemic level of uric acid, and has the ability to inhibit the renal tubular secretion of agents that are co-administered with it. In this study, we evaluated the effects of PRB co-administered with mizoribine (MZR) on the pharmacokinetics (PK) of MZR in 12 patients with nephrotic syndrome. The elimination rate constant (k_el) was used as an indicator of changes in the PK of MZR when the secretion of MZR was inhibited by co-administration of PRB, in order to determine the extent to which MZR was influenced by PRB. In 4 of the 12 patients studied, k_el decreased and the biological half-life (t_1/2) of MZR was prolonged when co-administered with PRB, in comparison with the values when MZR was used alone, thus revealing that the PK of MZR was influenced by PRB. Co-administration of PRB with MZR appears to be effective in prolonging the biological half-life of MZR and enhancing its effect in patients with nephrotic syndrome, although further studies will be required to determine the optimal dosage of PRB and renoprotective effects.Correspondence to:
Y. Utsunomiya, MD, PhD
Division of Kidney and Hypertension
Department of Internal Medicine
The Jikei University, School of Medicine
3-25-8, Nishi-Shimbashi, Minato-ku
Tokyo, 105-8461 Japan
Email: [email protected]

Abstract

Clinical Nephrology, Vol. 76 – No. 1/2011 (78-82)

Two cases of nephrotic syndrome (NS)-induced acute kidney injury (AKI) associated with renal hypouricemia

Y. Takeda¹, A. Abe¹, S. Nakanishi¹, M. Umezu¹, K. Hirano², H. Hayakawa², I. Ohno², K. Ichida², Y. Yamaguchi³, T. Hosoya² and M. Fukagawa¹

¹Division of Nephrology and Kidney Center, Kobe University School of Medicine, Hyogo, ²Division of Kidney and Hypertension, Department of Internal Medicine, Jikei University School of Medicine, Tokyo, and ³Yamaguchi’s Pathology Laboratory, Matsudo, Japan
Renal hypouricemia is a clinical disorder attributed to an increased renal urate excretion rate and is well known to involve a high risk of urolithiasis and exercise-induced acute kidney injury (AKI). This report concerns two interesting cases of nephrotic syndrome (NS)-induced AKI associated with renal hypouricemia. A 64-year-old female (Case 1) and a 37-year-old male (Case 2) were hospitalized because of AKI (serum creatinine: 2.07 mg/dl and 3.3 mg/dl, respectively), oliguria and NS. They were treated with prednisolone and temporary hemodialysis. Renal function improved, but hypouricemia persisted during hospitalization. Histological findings in both cases led to a diagnosis of minimal change nephrotic syndrome and identification of the diuretic phase of tubulointerstitial damage because of findings such as acute tubular necrosis. Furthermore, distal tubules of Case 2 showed an amorphous mass, possibly a uric acid crystal. Analysis of the two cases with the URAT1 gene, encoded by SLC22A12, found a homozygous mutation in exon 4 (W258stop) of each one. Our cases show that patients with renal hypouricemia may be susceptible to AKI without involvement of exercise if they possess some facilitators. Renal hypouricemic patients should therefore be carefully examined for all complications from renal hypouricemia because of high risk of AKI.Correspondence to:
M. Fukagawa, MD, PhD, FJSIM, FASN
Professor of Medicine
Division of Nephrology, Endocrinology and Metabolism
Tokai University School of Medicine
143 Shimo-Kasuya
Isehara, 259-1193, Japan
Email: [email protected]

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