Familial Renal Glucosuria and SGLT2

Santer, René; Calado, Joaquim

doi:10.2215/cjn.04010609

Cited by 315 publications

(297 citation statements)

References 69 publications

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“…In particular, all analyses using uromodulin to creatinine ratios were done using this transformation, and the corresponding figures use a log-transformed axis for uromodulin. Glycosuria, which was present in a minority of individuals, could not be normalized and was, therefore, dichotomized as present or absent on the basis of a 0.5-g/g creatinine cutoff (29).…”

Section: Statistical Analysesmentioning

confidence: 99%

“…We excluded three with a known history of renal disease. The remaining 943 were 5469 years old, with 51% women and a body mass index (BMI) of 26 (23)(24)(25)(26)(27)(28)(29)(30) (Table 1); 83% were white, 5% had a parent from Africa, 1% had a parent from Latin America, 4% had a parent from the Middle East, 2% were Asian, and 5% were from another descent. Cardiovascular risk factors and history were prevalent: 28% reported hyperlipidemia, 17% reported hypertension, 11% reported diabetes, and 6.7% had a history of coronary artery disease or stroke.…”

Section: Cohort Characteristicsmentioning

confidence: 99%

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Clinical, Genetic, and Urinary Factors Associated with Uromodulin Excretion

Troyanov

Delmas-Frenette

Bollée

et al. 2016

Clinical Journal of the American Society of Nephrology

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Background and objectives The urinary excretion of uromodulin is influenced by common variants in the UMOD gene, and it may be related to NaCl retention and hypertension. Levels of uromodulin are also dependent of the renal function, but other determinants remain unknown.Design, setting, participants, & measurements We tested associations between the urinary excretion of uromodulin; medical history and medication; serum and urinary levels of electrolytes, glucose, and uric acid; and the genotype at the UMOD/Protein Disulfide Isomerase-Like, Testis Expressed locus (rs4293393 and rs12446492); 943 participants from the CARTaGENE Cohort, a random sample from the Canadian population of 20,004 individuals, were analyzed. Participants with available genotyping were obtained from a substudy addressing associations between common variants and cardiovascular disease in paired participants with high and low Framingham risk scores and vascular rigidity indexes.Results The population studied was 5469 years old, with 51% women and eGFR of 9614 ml/min per 1.73 m 2 . Uromodulin excretion was 25 (11-42) mg/g creatinine. Using linear regression, it was independently higher among patients with higher eGFR, the TT genotype of rs4293393, and the TT genotype of rs12446492. The fractional excretions of urate and sodium showed a strong positive correlation with uromodulin, likely linked to the extracellular volume status. The presence of glycosuria and the use of uricosuric drugs, which both increased the fraction excretion of urate, were independently associated with a lower uromodulin excretion, suggesting novel interactions between uric acid and uromodulin excretion. ConclusionsIn this large cohort, the excretion of uromodulin correlates with clinical, genetic, and urinary factors. The strongest associations were between uric acid, sodium, and uromodulin excretions and are likely linked to the extracellular volume status.

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Section: Statistical Analysesmentioning

confidence: 99%

Section: Cohort Characteristicsmentioning

confidence: 99%

Clinical, Genetic, and Urinary Factors Associated with Uromodulin Excretion

Troyanov

Delmas-Frenette

Bollée

et al. 2016

Clinical Journal of the American Society of Nephrology

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“…It has been suggested that one possible mechanism of cisplatin-induced proximal tubule toxicity is reduced expression of SGLTs [121,123]. However, in patients with familial renal glucosuria (mutations in SGLT1/SGLT2 coding gene, SLC5A2), no acid-base homeostasis disturbances have been reported [124,125].…”

Section: Oxaplatin and Cisplatinmentioning

confidence: 99%

Drug-induced acid-base disorders

et al. 2014

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The incidence of acid-base disorders (ABDs) is high, especially in hospitalized patients. ABDs are often indicators for severe systemic disorders. In everyday clinical practice, analysis of ABDs must be performed in a standardized manner. Highly sensitive diagnostic tools to distinguish the various ABDs include the anion gap and the serum osmolar gap. Drug-induced ABDs can be classified into five different categories in terms of their pathophysiology: (1) metabolic acidosis caused by acid overload, which may occur through accumulation of acids by endogenous (e.g., lactic acidosis by biguanides, propofol-related syndrome) or exogenous (e.g., glycol-dependant drugs, such as diazepam or salicylates) mechanisms or by decreased renal acid excretion (e.g., distal renal tubular acidosis by amphotericin B, nonsteroidal antiinflammatory drugs, vitamin D); (2) base loss: proximal renal tubular acidosis by drugs (e.g., ifosfamide, aminoglycosides, carbonic anhydrase inhibitors, antiretrovirals, oxaliplatin or cisplatin) in the context of Fanconi syndrome; (3) alkalosis resulting from acid and/or chloride loss by renal (e.g., diuretics, penicillins, aminoglycosides) or extrarenal (e.g., laxative drugs) mechanisms; (4) exogenous bicarbonate loads: milk-alkali syndrome, overshoot alkalosis after bicarbonate therapy or citrate administration; and (5) respiratory acidosis or alkalosis resulting from drug-induced depression of the respiratory center or neuromuscular impairment (e.g

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“…동물실험 에서 당뇨병 쥐 모델에서 losartan 치료에 의해서 SGLT2 발현이 감소했다는 보고가 있다 [27]. 반면에 familial renal glycosuria 환자에서는 RAAS축의 활 성이 증가되어 있다는 보고들이 있으며 당뇨병 환자에 서 SGLT2 억제제 투여 시 혈압감소와 과여과의 감소 등 이로운 혈역학적 변화와 동반해서 레닌-안지오텐신 알도스테론 축의 활성이 증가한다고 보고되었다 [10,28]. 또한 RAAS 차단제와 SGLT2 억제제가 각 약 제의 단독요법 보다 신장보호효과가 더 우수하다는 동 물실험 결과가 있으므로 향후 임상연구를 통해서 확인 할 필요가 있다 [10,23].…”

Section: 레닌-안지오텐신-알도스테론 축의 변화unclassified

The Non-glycemic Effects of SGLT2 Inhibitor

Lee

2014

J Korean Diabetes

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Sodium glucose cotransporter 2 (SGLT2) inhibitors have recently been introduced as a new class of antidiabetic agents. In addition to their glycemic action, SGLT2 inhibitors also have a number of non-glycemic effects that may contribute to renal and/or cardiovascular benefits. These include effects on tubuloglomerular feedback in the kidney, body weight, blood pressure, and serum uric acid. Other non-glycemic effects of SGLT2 inhibitors that need to be further studied include the effects on lipid profiles, food intake, and secretion of hormones such as leptin, incretins, and aldosterone. Also, the exact mechanisms of various non-glycemic actions should be further studied. Additionally, SGLT2 inhibitor therapy in combination with other drugs may have beneficial glycemic and non-glycemic effects. (

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Familial Renal Glucosuria and SGLT2

Cited by 315 publications

References 69 publications

Clinical, Genetic, and Urinary Factors Associated with Uromodulin Excretion

Clinical, Genetic, and Urinary Factors Associated with Uromodulin Excretion

Drug-induced acid-base disorders

The Non-glycemic Effects of SGLT2 Inhibitor

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