熊谷 直憲

Citrate supplementation is well known to alleviate muscle fatigue. Furthermore, our previous clinical study revealed that citrate supplementation prevents renal oxidative stress and dysfunction. We hypothesize that an interaction between muscle and kidney tissues underlies the effects of citrate supplementation. This study investigated the effects of a citrate agent, potassium citrate/sodium citrate (PCSC), on muscle and renal functions. Male Sprague-Dawley rats were randomly assigned to two groups (control and PCSC groups). PCSC (2000 mg/kg body weight) was administered orally administrated for one week. Kidney weight, vastus lateralis muscle weight, and renal function were compared between the groups. Subsequently, the kidney and muscle tissues were analyzed using metabolomics. The PCSC group showed a significant increase in muscle mass relative to the weight gain (p = 0.0472). Renal function development with growth was more pronounced in the PCSC group (p < 0.0001). Metabolomic analysis of muscle tissue in the PCSC group revealed increased alanine levels and decreased levels of sarcosine, creatinine, and NADPH/NADP+ ratio. In the kidney tissue, PCSC supplementation led to elevated N,N-dimethylglycine, urea, and the ratio of malic acid to aspartate, while betaine aldehyde, carnitine, and Fisher's ratio decreased. The study concluded that PCSC supplement facilitated muscle growth metabolically through an alanine-associated pathway and renal function development by increasing intrarenal urea and accelerating the malate-shuttle and the betaine pathway. These findings indicate PCSC's potential impact of PCSCs on muscle-kidney interactions.

We report a case of tubulointerstitial nephritis with uveitis (TINU) diagnosed from isolated glucosuria detected during school urinary screening. The patient was a 12-year-old girl in whom glucosuria was detected during school urinary screening using a dipstick; however, urinary protein and occult blood were negative. There were no preceding symptoms of infection or medication. The patient visited the Fujita Health University Okazaki Medical Center two weeks after the school urinary screening for further examination. No edema or skin rash was observed. A urine test showed urinary glucose was positive and urinary β2-microglobulin was high; other values were almost normal. Mild renal dysfunction was observed. There was no hyperglycemia or high HbA1c level; therefore, diabetes mellitus was ruled out. Various autoantibody tests were negative, and the angiotensinogen-converting enzyme level was within the normal range. The patient was clinically diagnosed with idiopathic tubulointerstitial nephritis without a renal biopsy. Renal dysfunction tended to improve gradually after the first visit. Three months after the first visit, conjunctival congestion appeared in the right eye, and the patient was diagnosed with uveitis and eventually with TINU. When performing detailed examinations for urinary glucose, it is necessary to differentiate kidney disease as well as diabetes mellitus. Moreover, it is necessary to recognize that even if the urine dipstick test is negative for protein, it may be positive for low-molecular-weight protein.