Change over Time in the Risk of Death among Japanese COVID-19 Cases Caused by the Omicron Variant Depending on Prevalence of Sublineages.

To assess temporal changes to the risk of death in COVID-19 cases caused by the Omicron variant, we calculated age-standardized case fatality rates (CFR) in patients aged ≥40 years over nine diagnostic periods (3 January to 28 August 2022) in ten Japanese prefectures (14.8 million residents). Among 552,581 study subjects, we found that there were 1836 fatalities during the isolation period (up to 28 days from date of onset). The highest age-standardized CFR (0.85%, 95% confidence interval (CI):0.78-0.92) was observed in cases diagnosed in the second 4-week period (January 31 to February 27), after which it declined significantly up to the 6th 4-week period (0.23%, 95% CI: 0.13-0.33, May 23 to June 19). The CFR then increased again but remained at 0.39% in the eighth period (July 18 to August 28). The CFR in cases with the BA.2 or BA.5 sublineages in the age range 60-80 years was significantly lower than that with BA.1 infections (60 years: 0.19%, 0.02%, 0.053%, respectively; 70 years: 0.91%, 0.33%, 0.39%; ≥80 years: 3.78%, 1.96%, 1.81%, respectively). We conclude that the risk of death in Japanese COVID-19 patients infected with Omicron variants declined through February to mid-June 2022.

Blockade of Acid-Sensing Ion Channels Increases Urinary Bladder Capacity With or Without Intravesical Irritation in Mice.

We conducted this study to examine whether acid-sensing ion channels (ASICs) are involved in the modulation of urinary bladder activity with or without intravesical irritation induced by acetic acid. All in vivo evaluations were conducted during continuous infusion cystometry in decerebrated unanesthetized female mice. During cystometry with a pH 6.3 saline infusion, an i.p. injection of 30 µmol/kg A-317567 (a potent, non-amiloride ASIC blocker) increased the intercontraction interval (ICI) by 30% (P < 0.001), whereas vehicle injection had no effect. An intravesical acetic acid (pH 3.0) infusion induced bladder hyperactivity, with reductions in ICI and maximal voiding pressure (MVP) by 79% (P < 0.0001) and 29% (P < 0.001), respectively. A-317567 (30 µmol/kg i.p.) alleviated hyperreflexia by increasing the acid-shortened ICI by 76% (P < 0.001). This dose produced no effect on MVP under either intravesical pH condition. Further analysis in comparison with vehicle showed that the increase in ICI (or bladder capacity) by the drug was not dependent on bladder compliance. Meanwhile, intravesical perfusion of A-317567 (100 µM) had no effect on bladder activity during pH 6.0 saline infusion cystometry, and drug perfusion at neither 100 µM nor 1 mM produced any effects on bladder hyperreflexia during pH 3.0 acetic acid infusion cystometry. A-317567 has been suggested to display extremely poor penetrability into the central nervous system and thus to be a peripherally active blocker. Taken together, our results suggest that blockade of ASIC signal transduction increases bladder capacity under normal intravesical pH conditions and alleviates bladder hyperreflexia induced by intravesical acidification and that the site responsible for this action is likely to be the dorsal root ganglia.

Corrigendum: Blockade of Acid-Sensing Ion Channels Increases Urinary Bladder Capacity With or Without Intravesical Irritation in Mice.

[This corrects the article DOI: 10.3389/fphys.2020.592867.].

Urothelial ATP exocytosis: regulation of bladder compliance in the urine storage phase.

The bladder urothelium is more than just a barrier. When the bladder is distended, the urothelium functions as a sensor to initiate the voiding reflex, during which it releases ATP via multiple mechanisms. However, the mechanisms underlying this ATP release in response to the various stretch stimuli caused by bladder filling remain largely unknown. Therefore, the aim of this study was to elucidate these mechanisms. By comparing vesicular nucleotide transporter (VNUT)-deficient and wild-type male mice, we showed that ATP has a crucial role in urine storage through exocytosis via a VNUT-dependent mechanism. VNUT was abundantly expressed in the bladder urothelium, and when the urothelium was weakly stimulated (i.e. in the early filling stages), it released ATP by exocytosis. VNUT-deficient mice showed reduced bladder compliance from the early storage phase and displayed frequent urination in inappropriate places without a change in voiding function. We conclude that urothelial, VNUT-dependent ATP exocytosis is involved in urine storage mechanisms that promote the relaxation of the bladder during the early stages of filling.

Congenital prepubic sinus accompanied by prevesical abscess.

Congenital prepubic sinus is an extremely rare anomaly. The etiology is uncertain and the anatomical features often differ from each other. We report a 22-year-old woman with a congenital prepubic sinus accompanied by a prevesical abscess. She was admitted to our hospital with high-grade fever and low abdominal pain. Computed tomography revealed a prevesical abscess. After treatment of the prevesical abscess, we completely excised the congenital prepubic sinus. To our knowledge, this is the first reported case that accompanied by prevesical abscess on a congenital prepubic sinus. Moreover, this case represents the oldest reported age of a patient with a congenital prepubic sinus.

[Questionnaire survey on medical care for male urethritis in community clinics in Shiga prefecture].

Six regional medical associations in Shiga prefecture agreed to cooperate in an investigation of medical care for male gonococcal and chlamydial urethritis. In June 2011, we sent a questionnaire to 372 medical offices in Shiga prefecture, and analyzed replies of respondents. Ten urologists and 175 non-urologists responded to the survey (response rate 49.7%). Among 185 physicians, 52 (10 urologists and 42 nonurologists) have treated male patients with gonococcal and chlamydial urethritis. More than 20% (42/175) of non-urological clinics are involved in the medical management. At initial diagnosis for sexually transmitted male urethritis, all urologists select the nucleic acid amplification method (100%), whereas many non-urologists do not (35%). For the treatment of chlamydial urethritis, non-urologists select levofloxacin (LVFX, 52.8%) rather than azithromycin (AZM, 22.0%), whereas urologists use AZM (78.0%) mostly but do not use LVFX (0%) (p = 0.023). For the treatment of gonococcal urethritis, non-urologists prefer oral new quinolones (53.1%) compared to urologists (25.0%) (p = 0. 74). For cure judgment of gonoccocal and chlamydial urethritis, many non-urologists rely on the improvement of subjective symptoms (50 and 47%), but urologists do not (10 and 0%) (p = 0.022 and 0.026, respectively). As for recognition of the clinical guideline for sexually transmitted disease, most urologists (90%) know it, but few non-urologists (13%) do (p < 0.001). We found that non-urological clinics make a great contribution to the medical treatment for male gonococcal and chlamydial urethritis in Shiga prefecture. It is important to standardize the medical care for sexually transmitted male urethritis by familiarizing non-urological practitioners with the clinical guideline.

Muscarinic receptor binding of the novel radioligand, [3h]imidafenacin in the human bladder and parotid gland.

The aim of the current study was to demonstrate highly specific and direct binding activity of tritium ([(3)H])-labeled imidafenacin for labeling muscarinic receptors in human bladder and parotid gland. Specific binding of [(3)H]imidafenacin in human tissues was saturable, reversible, and of high affinity. The Kd value for specific [(3)H]imidafenacin binding in the human bladder was approximately 3 times higher than that in the parotid gland. Unlabeled imidafenacin as well as the clinically used antimuscarinic agents, oxybutynin, tolterodine, and solifenacin, competed with [(3)H]imidafenacin for binding sites in the human bladder and parotid gland in a concentrationdependent manner, which indicated pharmacological specificity of [(3)H]imidafenacin binding sites. The Ki for imidafenacin in the human bladder approximately corresponded to pharmacological potency for the competitive blockade of carbachol-induced contractions of bladder, indicating a close correlation between binding affinity of imidafenacin to bladder muscarinic receptors and its pharmacological effects in the bladder. In conclusion, the current study is the first to provide direct evidence to demonstrate that imidafenacin bound muscarinic receptors in the human bladder, supporting its clinical relevance as a therapeutic agent for overactive bladder. [(3)H]Imidafenacin may also be a useful radioligand for labeling the M3 subtype of muscarinic receptors with higher selectivity than other radioligands.

Eviprostat activates cAMP signaling pathway and suppresses bladder smooth muscle cell proliferation.

Eviprostat is a popular phytotherapeutic agent for the treatment of lower urinary tract symptoms (LUTS). At present, the signaling mechanisms underlying its therapeutic effects are still poorly understood. Given that cAMP has been reported to suppress cell hyperplasia and hypertrophy in various pathological situations, we asked whether the effect of Eviprostat could be ascribed to the activation of the cAMP signaling pathway. In the study, exposure of cAMP response element (CRE)-secreted alkaline phosphatase (SEAP) (CRE-SEAP)-reporter cells to Eviprostat elevated SEAP secretion, which was associated with an increased phosphorylation of vasodilator-stimulated phosphoprotein (VASP) and cAMP-response element-binding protein (CREB), as well as enhanced expression of CRE-regulated protein connexin43, indicating an activation of the cAMP signaling pathway. Consistent with these observations, Eviprostat-induced expression of Cx43 was abolished in the presence of adenylyl cyclase inhibitor SQ22536 or PKA inhibitor H89, whereas it was mimicked by adenylyl cyclase activator, forskolin. Further analysis demonstrated that Eviprostat significantly potentiated the effect of phosphodiesterase 3 (PDE3) inhibitor, but not that of PDE4 inhibitor, on CRE activation. Moreover, Eviprostat suppressed PDGF-induced activation of ERK and Akt and inhibited cell proliferation and hillock formation in both mesangial cells and bladder smooth muscle cells. Collectively, activation of the cAMP signaling pathway could be an important mechanism by which Eviprostat exerts its therapeutic effects for LUTS.

Fesoterodine, its active metabolite, and tolterodine bind selectively to muscarinic receptors in human bladder mucosa and detrusor muscle.

OBJECTIVE: To comparatively characterize the binding activity of fesoterodine, its active metabolite (5-hydroxymethyl tolterodine [5-HMT]), and tolterodine in the human bladder mucosa, detrusor muscle, and parotid gland. MATERIALS AND METHODS: Muscarinic receptors in the homogenates of human bladder mucosa, detrusor muscle, and parotid gland were measured by a radioligand binding assay using [N-methyl-(3)H] scopolamine methyl chloride. RESULTS: Fesoterodine, 5-HMT, and tolterodine competed with [N-methyl-(3)H] scopolamine methyl chloride for binding sites in the bladder mucosa, detrusor muscle, and parotid gland in a concentration-dependent manner. The affinity for muscarinic receptors of these agents was significantly greater in the bladder than in the parotid gland, suggesting pharmacologic selectivity for the bladder over the parotid gland. The bladder selectivity was larger for fesoterodine and 5-HMT than for tolterodine. Fesoterodine, 5-HMT, and tolterodine resulted in significantly increased (two- to five-fold) values of the apparent dissociation constant for specific [N-methyl-(3)H] scopolamine methyl chloride binding in the detrusor muscle and parotid gland, with little effect on the corresponding values of the maximal number of binding sites. This finding indicates that these agents bind to the human muscarinic receptors in a competitive and reversible manner. CONCLUSION: Fesoterodine and 5-HMT bind to the muscarinic receptors with greater affinity in the human bladder mucosa and detrusor muscle than in the parotid gland in a competitive and reversible manner.

[Small intestinal metastasis from renal cell carcinoma: a case report].

A 52-year-old man who had been treated with sorafenib for lung metastasis of renal cell carcinoma (RCC) presented to our hospital with iron-deficiency anemia. He had undergone right nephrectomy for RCC (clear cell carcinoma, pT1bN0M0) 11 years ago and lung metastasis developed 6 years after the surgery. Although upper gastrointestinal endoscopy and colonoscopy were performed on suspicion of gastrointestinal bleeding, no abnormality was detected. Capsule endoscopy and single balloon small bowel endoscopy disclosed a hemorrhagic submucosal tumor in the jejunum. Laparoscopic partial jejunectomy was performed, and pathological examination indicated metastatic RCC to the small intestine. After the operation, anemia improved but he died 8 months later because of intrabronchial bleeding from the metastatic lesion of the lung. Metastatic RCC of the small intestine is relatively rare, its diagnosis is difficult. Recently, new diagnostic tools such as capsule endoscopy and balloon-assisted endoscopy have been developed, and they are useful in diagnosing gastrointestinal bleeding (OGIB) which can not be detected by traditional enteroscopy. If patients with advanced RCC show gastrointestinal bleeding of uncertain etiology, we should perform aggressive examination of the digestive tract with these diagnostic tools.

Decreased expression of the epithelial Ca2+ channel TRPV5 and TRPV6 in human renal cell carcinoma associated with vitamin D receptor.

PURPOSE: We investigated the expression of epithelial Ca(2+) channel TRPV (transient receptor potential vanilloid subfamily) 5 and 6, and vitamin D receptor in primary human renal cell carcinoma and benign peritumor tissues, and assessed the possible association between TRPV5/6 and vitamin D receptor expression. MATERIALS AND METHODS: Fresh-frozen primary tumor and peritumor tissues from 27 patients diagnosed with renal cell carcinoma were analyzed for TRPV5/6 and vitamin D receptor expression by quantitative reverse transcriptase-polymerase chain reaction, Western blot and immunohistochemistry. RESULTS: Quantitative reverse transcriptase-polymerase chain reaction revealed that TRPV5/6 and vitamin D receptor expression was decreased 38.11, 4.44 and 3.20 times in renal cell carcinoma vs normal kidney tissue (p = 0.012, 0.002 and 0.020, respectively). Relatively higher expression was noted for chromophobe renal cell carcinoma than for the other renal cell carcinoma subtypes. Vitamin D receptor mRNA expression significantly correlated with that of TRPV6 (r = 0.508, p = 0.007) and TRPV5 (r = 0.697, p = 0.032) in renal cell carcinoma. Western blot showed results similar to those of reverse transcriptase-polymerase chain reaction. Different expression was detected between kidney and renal cell carcinoma tissue. Immunohistochemical analysis verified strong detection of TRPV5/6 and vitamin D receptor in distal nephrons but demonstrated weak or no immunostaining much more often in renal cell carcinoma. CONCLUSIONS: Decreased TRPV5/V6 expression was noted in renal cell carcinoma, which correlated with vitamin D receptor. Different expression was also detected among the different renal cell carcinoma histopathological subtypes. Our observations suggest that altered vitamin D receptor expression may be associated with renal cell carcinoma carcinogenesis via TRPV5/6.

Bladder outlet obstruction induced expression of prostaglandin E2 receptor subtype EP4 in the rat bladder: a possible counteractive mechanism against detrusor overactivity.

PURPOSE: Prostaglandins have been implicated as endogenous modulators of bladder function under physiological and pathological conditions. We examined how the expression of each EP receptor subtype changed in association with bladder outlet obstruction and focused on the functional role of EP4 receptor subtype in the bladder with outlet obstruction. MATERIALS AND METHODS: We assessed the gene expression of EP receptor subtypes by reverse transcriptase-polymerase chain reaction. EP4 protein localization was determined by immunohistochemistry. The effect of the selective EP4 agonist ONO-AE1-329 on 50 mM KCl induced contraction of rat bladder strips was examined in vitro. Continuous infusion cystometrograms were done to examine the effect of intravesical perfusion of ONO-AE1-329 on the micturition reflex in urethane anesthetized rats. RESULTS: EP4 receptor genes were largely expressed in bladders with outlet obstruction but absent in controls. EP4 receptor proteins were clearly detected in obstructed bladder detrusor smooth muscle and epithelium. ONO-AE1-329 (100 µM) significantly relaxed KCl induced contraction of bladder strips from rats with bladder outlet obstruction. A significant correlation was found between the relaxant effect of ONO-AE1-329 and whole bladder weight. In rats with bladder outlet obstruction intravesical infusion of 10 µM ONO-AE1-329 significantly increased bladder capacity without changing micturition pressure while it had no effect in controls. CONCLUSIONS: Activation of the EP4 receptors expressed in bladders with outlet obstruction may suppress detrusor muscle contraction and afferent activity. This might be a compensatory mechanism to counteract the deterioration of storage function in bladders with outlet obstruction.

Characterization of muscarinic receptors in the human bladder mucosa: direct quantification of subtypes using 4-DAMP mustard.

OBJECTIVE: To characterize pharmacologically relevant muscarinic receptors in the human bladder mucosa and detrusor muscle using radioligand binding assays with [N-methyl-3H]scopolamine methyl chloride ([3H]NMS) and 4-DAMP mustard. METHODS: Muscarinic receptors in homogenates of bladder mucosa, detrusor muscle, and parotid gland were measured using the radioligand [3H]NMS. 4-DAMP mustard was used to inactivate M3 receptors irreversibly. RESULTS: Specific [3H]NMS binding in the homogenates of the mucosa and detrusor muscle was saturable and of high affinity as shown by dissociation constants (Kd) of 260 ±82 and 237 ±49 pM, respectively. Antimuscarinic agents (oxybutynin, propiverine, tolterodine, and darifenacin) and their active metabolites competed with [3H]NMS for the binding sites in the human mucosa in a concentration-dependent manner. These agents exhibited similar affinity in the detrusor muscle. The Bmax. values of [3H]NMS in the detrusor, bladder mucosa, and parotid gland were significantly decreased by pretreatment with 4-DAMP mustard (36%, 41% and 63%, respectively). CONCLUSION: The density and binding affinity profile of the muscarinic receptor population in the human bladder mucosa was shown to be similar to that of the detrusor muscle. The density of the M3 subtype in the mucosa was similar to that in the detrusor muscle but lower than that in the parotid gland.

Muscarinic Receptor Binding of Imidafenacin in the Human Bladder Mucosa and Detrusor and Parotid Gland.

OBJECTIVES: The current study aimed to characterize comparatively the binding of imidafenacin to muscarinic receptors in the human bladder mucosa and detrusor muscle and parotid gland. METHODS: The muscarinic receptor in homogenates of human tissues (bladder mucosa and detrusor muscle and parotid gland) was measured using a radioligand binding assay with [N-methyl-(3) H]scopolamine methyl chloride ([(3) H]NMS). RESULTS: Imidafenacin competed with [(3) H]NMS for binding sites in the bladder mucosa and detrusor muscle and parotid gland, and its affinity was significantly (2.6-8.7 times) higher than that of oxybutynin. Also, the affinity of imidafenacin for muscarinic receptors was approximately two-fold higher in the parotid gland than bladder tissue. The affinity of imidafenacin in the mucosa was similar to that in the detrusor muscle, suggesting that this agent exhibits therapeutic effects by blocking muscarinic receptors in the mucosa as well as detrusor muscle. Scatchard analysis revealed that imidafenacin increased significantly (approximately four-fold) Kd values for [(3) H]NMS binding in the human detrusor muscle and parotid gland, with little effect on Bmax values. This observation indicates that imidafenacin binds to the muscarinic receptors in human tissues in a competitive and reversible manner. CONCLUSION: Imidafenacin binds to muscarinic receptors in the human bladder mucosa and detrusor muscle and parotid gland with high affinity. This agent was considered to exhibit therapeutic effects on the lower urinary tract symptoms due to an overactive bladder by blocking muscarinic receptors in the urothelium as well as detrusor muscle.

Predictive factors for the effect of the α1-D/A adrenoceptor antagonist naftopidil on subjective and objective criteria in patients with neurogenic lower urinary tract dysfunction.

OBJECTIVES: • To assess the effect of α1-D/A adrenoceptor antagonist naftopidil on patients with neurogenic lower urinary tract dysfunction (NLUTD) and voiding difficulty. • To explore the effectiveness of naftopidil in these patients by using urodynamic variables, including pressure flow study (PFS), and to find good and simple parameters (International Prostate Symptom Score (IPSS), Post-void residual urine (PVR), and uroflowmetry (UFM) parameters) as substitution of PFS for predicting the effect of naftopidil. PATIENTS AND METHODS: • The main inclusion and exclusion criteria were, IPSS ≥8, voiding symptoms with IPSS ≥5, IPSS-quality of life (QOL) ≥2, PVR ≥50 mL, and without prostatic enlargement ≥ 20 mL. • After initial assessment, patients were stepwisely administered for 12 weeks with the following: placebo for 2 weeks, naftopidil 25 mg/day for 2 weeks, naftopidil 50 mg/day for 2 weeks, and naftopidil 75 mg/day for 6 weeks. At the end of both placebo and 6 weeks' naftopidil 75 mg/day, their IPSS, UFM, PVR, and PFS were assessed. • A total of 82 Japanese patients (men 40, women 42) with lower urinary tract symptoms complicated by NLUTD, with a mean age of 63.9 years, were included from private or institutional clinics. • The lesions were spinal cord 42, and peripheral nervous system 40. The spinal cord lesions were all lumbar spine (injury or lumbar canal stenosis). RESULTS: • In all patients, pressure at maximum urinary flow rate (P(det) Q(max) ) in PFS significantly decreased (P < 0.05), and maximum urinary flow rate in UFM significantly increased (P < 0.01). Analysis of data for men and for women also showed a significant decrease in PVR, %PVR, and total IPSS score. • The degree of improvement of voided volume, PVR (%), and IPSS in patients with PVR <300 mL was significantly greater than those in patients with PVR ≥300 mL. • The degree of improvement of P(det) Q(max) in PFS, and IPSS in patients with bladder contractility was significantly greater than that in patients without bladder contractility. CONCLUSIONS: • α1-D/A adrenoceptor antagonist naftopidil has a significant effect on both symptoms and urodynamic variables of patients of both genders with NLUTD in Japan. • PVR <300 mL and bladder contractility are predictive factors for the efficacy of naftopidil on patients with NLUTD.

Functional roles of TRPV1 channels in lower urinary tract irritated by acetic acid: in vivo evaluations of the sex difference in decerebrate unanesthetized mice.

Sex-specific differences in activity of the lower urinary tract (LUT) responding to acid irritation in mice have been revealed. This study, using continuous infusion cystometry with acetic acid (AA; pH 3.0), was conducted to examine whether the transient receptor potential vanilloid type 1 (TRPV1) channels expressed in the mouse LUT are involved in the sex difference in functional responses of the bladder and urethra to irritation. No differences were found between effects of capsazepine (a TRPV1 blocker; 100 microM) and those of its vehicle on any of the cystometric changes by intravesical AA in either female or male mice. However, capsazepine eliminated the acid-induced sex differences in parameters associated with bladder contraction phase (i.e., maximal voiding pressure, closing peak pressure, 2nd-phase contraction, bladder contraction duration), whereas capsazepine did not affect those in parameters associated with bladder-filling period (i.e., intercontraction interval, actual collecting time). In males, capsazepine reduced the number of bladder contractions accompanying fluid dribbling at 2nd-phase contraction, which is indicative of the urethral response to irritation, whereas in females it increased the number. Together, these results suggest the possibilities that TRPV1 channels in the bladder and urethra are involved in the sex difference in the LUT response to acid irritation and that these participate, e.g., via "cross talk" between the bladder and urethra, in the fine-tuning of intravesical pressure (or bladder emptying) at the bladder contraction phase under irritated LUT conditions but not in sensing for bladder filling during the storage period, although the contribution of the mechanism may be small.

The forefront for novel therapeutic agents based on the pathophysiology of lower urinary tract dysfunction: pathophysiology of voiding dysfunction and pharmacological therapy.

Normal lower urinary tract function consists of voiding and storage. During voiding, the pontine micturition reflex center orders the sacral parasympathetic nucleus to increase parasympathetic activity, resulting in urinary bladder detrusor contraction via activation of post-synaptic muscarinic receptors (M2/3) and in the relaxation of both urethral and prostatic smooth muscle by nitric oxide (NO). In addition, the rhabdosphincter relaxes by inhibition of the pudendal nucleus at the sacral portion. During the storage phase, increase in sympathetic activity relaxes the urinary bladder via activation of post-synaptic beta(3)-receptors and in the contraction of both urethral and prostatic smooth muscles via alpha(1)-adrenoceptor. Many factors influence voiding function, including lower urinary tract disorders (benign prostatic hyperplasia in males, urethral stricture) and neurological disorders (central and peripheral). Theories of pharmacotherapy for voiding dysfunction are 1) increase detrusor contractility and 2) decrease urethral resistance. The former includes agonists for muscarinic receptors and cholinesterase inhibitor; and the latter includes alpha(1)-adrenoceptor antagonists, NO donors, benzodiazepines, baclofen, dantrolene, and boturinum toxin.

[Two cases of infants with acute renal failure due to bilateral obstructive ureteral stones associated with rotavirus gastroenteritis].

We report on 2 infants with acute renal failure caused by bilateral obstructive ureteral stones associated with rotavirus gastroenteritis. A 28-month boy and a 13-month boy with several days history of watery diarrhea and vomiting were referred to our hospital because of anuria. They were diagnosed acute post-renal failure due to obstructive bilateral ureteral stones based on the findings of ultrasound scan and computed tomography. Immediately, percutaneous nephrostomy tubes were inserted for urinary drainage, serum levels of creatinine and uric acid returned to normal within several days. Sandy stones were excreted through the nephrostomy tubes with urine after urinary alkalization, which were proved to be mainly ammonium acid urate. Ammonium acid urate is rare in developed countries, but some cases of bilateral urolithiasis causing acute renal failure in infants with rotavirus gastroenteritis were reported in recent years. It has been known that the cause of acute renal failure is renal azotemia resulting from sustained hypovolemia, but post-renal causes due to ammonium acid urate stones should be taken into consideration.