Association of kidney and cysts dimensions with anthropometric and biochemical parameters in patients with ADPKD

Abstract

The aim of the study was to evaluate an association between kidney and cyst dimensions and anthropometric, clinical and biochemical parameters of autosomal dominant polycystic kidney disease (ADPKD) patients. Forty-nine adults, ADPKD-diagnosed patients aged 36 ± 11 years, and 50 healthy controls were included in the study. Oral glucose tolerance test (OGTT with 75 g of glucose) was performed and venous blood was collected to measure biochemical parameters and various ion concentrations. Ultrasound abdominal examinations were performed with special emphasis on kidney and cysts parameters. In the ADPKD group, mean kidney length correlated positively with age, systolic blood pressure (SBP), diastolic blood pressure (DBP), fasting glucose and glucose and C-peptide concentrations after 120 min of glucose intake and negatively with Mg(2+) concentration and glomerular filtration rate (eGFR). Multivariate analyses adjusted for age and gender showed that higher mean kidney length and maximal cyst diameter were significant predictors of higher SBP (p = 0.034 and 0.046, respectively) and DBP (p = 0.024 and 0.034, respectively), higher maximal cyst diameter was a significant predictor of higher OGTT 2-h C-peptide concentration (p = 0.033), higher mean cyst diameter was a significant predictor of lower eGFR (p = 0.039) and higher mean kidney length was a significant predictor of lower serum magnesium concentration (p = 0.043). In the ADPKD patients with normal GFR, mean kidney length and mean cyst diameter measured by ultrasonography are associated negatively with GFR and positively with blood pressure. Higher mean kidney length and cyst diameter might be indicators of disorders of glucose and magnesium metabolism which precede renal failure in patients with ADPKD.

Hypomagnesaemia is absent in children with autosomal dominant polycystic kidney disease

“…4 One study in adult patients with ADPKD has found significantly lower concentrations of magnesaemia. 16 However, the authors did not give information about the prevalence of hypomagnesaemia. Furthermore, they included also patients with diuretics -a drug that is known to cause hypomagnesaemia; 5 therefore, lower concentrations of magnesaemia due to diuretic therapy cannot be excluded.…”

Inhibition of pannexin‐1 does not restore electrolyte balance in precystic Pkd1 knockout mice

“…The majority of the ADPKD patients has mutations in PKD1 or PKD2 , which encode polycystin‐1 (PC1) and polycystin‐2 (PC2), respectively (Cornec‐Le Gall et al., 2018 ). Although the exact prevalence is unknown, case reports indicate that ADPKD patients may also present with electrolyte abnormalities, including hypomagnesemia and hypo‐ or hypercalcemia (Pietrzak‐Nowacka et al., 2013 , 2015 ; Veeramuthumari & Isabel, 2013 ). However, the mechanism underlying the hypomagnesemia and hypocalcemia in APDKD remains elusive and is complicated by the fact that patients may be treated with different types of drugs, including diuretics against hypertension (Wuthrich et al., 2015 ).…”

Polycystin-1 dysfunction impairs electrolyte and water handling in a renal precystic mouse model for ADPKD

“…In advanced ADPKD, hypertension is common and glomerular filtration rate (GFR) is reduced (6,48). Electrolyte disturbances in ADPKD are described in literature, but these reports are mostly restricted to cystic ADPKD (4,11,13,34,39,40,43,44,47,51,55,57,58). When electrolyte imbalances are detected in cystic ADPKD, it is not possible to discern whether these disturbances are caused by dysfunctional PC1 or by cyst formation or defects in GFR, which dramatically impair renal fluid flow and blood filtration, respectively.…”