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Diabetes Mellitus, Obesity, Lipoprotein Disorders and other Metabolic Diseases
Published in John S. Axford, Chris A. O'Callaghan, Medicine for Finals and Beyond, 2023
Renal glycosuria is glycosuria occurring with a normal blood glucose level. This occurs when glucose in the renal filtrate is incompletely reabsorbed because of reduced function of the glucose-reabsorbing transporters in the renal tubules. The class of oral diabetes drugs sodium-linked glucose transporter 2 inhibitors (SGLT2i) lower blood glucose by causing glycosuria.
Endocrinology
Published in Fazal-I-Akbar Danish, Essential Lists of Differential Diagnoses for MRCP with diagnostic hints, 2017
Glycosuria:1 Diabetes mellitus.2 Renal glycosuria.16
The Nature of Renal Function
Published in Anthony R. Mundy, John M. Fitzpatrick, David E. Neal, Nicholas J. R. George, The Scientific Basis of Urology, 2010
Glucose is reabsorbed by cotransport with sodium, chiefly in the early proximal tubule. Glucose is not merely acting as an energy source for sodium transport, since the nonmetabolized glucose analogue α-methyl-d-glucoside can be substituted for it, but its transport is dependent on sodium reabsorption. At least two sodium-glucose cotransporters have been identified in mammalian proximal tubule; they have been named SGLT-1 and SGLT-2, respectively. SGLT-1 binds one sodium ion and one glucose molecule, while SGLT-2 has a stoichiometry of 2Na+:1 glucose. SGLT-2 is probably the more important of the two (29). It is saturable, and when the filtered load of glucose exceeds its maximal transporting capacity (Tm), the excess is excreted in the urine. The relationship between glucose filtration, reabsorption and excretion is shown in Figure 5. Glycosuria occurs in hyperglycemia (as in diabetes mellitus) because the filtered load of glucose exceeds the Tm of the transport system. Glycosuria because of abnormalities of the tubular glucose transport system (renal glycosuria) occurs when the renal threshold for glucose is less than the normalblood glucose concentration and is because of mutations in the gene for SGLT-2 (30).
Combined crystal-storing histiocytosis, light chain proximal tubulopathy, and light chain crystalline podocytopathy in a patient with multiple myeloma: a case report and literature review
Published in Renal Failure, 2023
Li Zhu, Lei Wang, Hongxia Shi, Lei Jiang, Xin Li, Chunying Shao, Yu Yan, Bao Dong, Wanzhong Zou, Li Zuo
Our patient presented with renal insufficiency and renal glycosuria. Although serum creatinine was significantly elevated, uric acid and serum phosphorus were normal, and hypokalemia persisted, which suggests the presence of Fanconi syndrome. Urinary protein was mainly low molecular weight protein, and albumin was also present. It was considered that the lesions mainly involved the proximal renal tubules and glomerulus. Due to the presence of monoclonal immunoglobulin, monoclonal gammopathy of renal significance (MGRS) or MM was suspected. Renal biopsy and bone puncture confirmed our hypothesis. It is suggested that monoclonal immunoglobulin-induced crystalline nephrology should be confirmed when Fanconi syndrome is complicated with monoclonal immunoglobulin. If there is evidence of glomerular involvement at the same time, caution should be taken with LCCP.
Inhibition of sodium-glucose cotransporter 2 to slow the progression of chronic kidney disease
Published in Acta Clinica Belgica, 2022
Fabie Oguz, Nathalie Demoulin, Jean Paul Thissen, Michel Jadoul, Johann Morelle
The important role of SGLT2 in the absorption of glucose by the kidney proximal tubule has been demonstrated by a series of experimental data and genetic studies in individuals with renal glucosuria. SGLT2 is highly expressed in the brush border of the early segment of the kidney proximal tubule and accounts for the reabsorption of 80%-90% of filtered glucose [7]. SGLT2 is responsible for the low affinity high capacity, sodium-dependent and phlorizin-sensitive glucose transport occurring in this segment of the nephron [7]. The role of SGLT2 in glucose homeostasis is further supported by the identification of homozygous or compound heterozygous variants in the SCL5A2 gene, which encodes for SGLT2, as the cause of renal glucosuria, a rare and benign condition characterized by urinary glucose excretion (60–120 g/day) with normal blood glucose levels [8,9].
The Association between Urinary Glucose and Renal Uric Acid Excretion in Non-diabetic Patients with Stage 1-2 Chronic Kidney Disease
Published in Endocrine Research, 2021
Xinhui Feng, Yuqi Zheng, Haochen Guan, Xun Zhou, Ying Xu, Xiaoli Zhang, Chensheng Fu, Jing Xiao, Zhibin Ye
In our study, we found that FEG and EgGF were positively correlated with EurGF in non-diabetic patients with stage 1–2 CKD by Pearson’s correlation and multiple linear regressions after adjusting for sex, age, BMI, urinary pH, eGFR, SUA, FBG, HbA1C and UACR. In a cross-sectional study of patients with non-diabetic advanced CKD, Hung et al revealed an association between glycosuria and increased FE of electrolytes, such as the FE of sodium and potassium and FEua.27 Moreover, in non-diabetic patients with stage 5 CKD, glycosuria was shown to result in a favorable renal outcome.27 In the context of euglycaemia, the reabsorption of filtered glomerular proteins could cause proximal tubular injury, and the defective renal proximal tubular reabsorption of glucose leads to glycosuria in non-diabetic CKD patients. However, glycosuria has not been reported to account for renal dysfunction in several case reports and animal models of hereditary renal glycosuria.42–44 No significant renal impairment has been associated with short-term SGLT2 inhibitor treatment,45,46 but the long-term outcomes of glycosuria remain unknown. The hypothesized mechanism of glycosuria in advanced CKD patients without diabetes is probably a consequence of an impairment of proximal tubular reabsorption.27 However, in our study, we eliminated advanced CKD patients with an eGFR<60 ml/min/1.73 m2 and still found an association between urinary glucose excretion and renal excretion of UA, indicating that the association was independent of the slight decrease in eGFR.