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Glycogenosis type I – von Gierke disease
Published in William L. Nyhan, Georg F. Hoffmann, Aida I. Al-Aqeel, Bruce A. Barshop, Atlas of Inherited Metabolic Diseases, 2020
William L. Nyhan, Georg F. Hoffmann, Aida I. Al-Aqeel, Bruce A. Barshop
A variety of renal complications has been observed. In addition to the renal Fanconi syndrome, patients have had distal renal tubular disease [52], amyloidosis [53], hypercalciuria, nephrocalcinosis, and calculi. Decrease in urinary citrate was found in 15 patients [54], reversing the normal increase with age, along with hypercalciuria. The authors suggested that treatment with citrate might be useful in preventing nephrocalcinosis and calculi. Glomerular hyperfiltration, increased renal plasma flow, and microalbuminuria [55] are followed over time by proteinuria, focal segmental glomerulosclerosis, and interstitial fibrosis [23, 56, 57]; followed in some patients by renal failure, leading to dialysis and transplantation.
Renal Cancer
Published in Manit Arya, Taimur T. Shah, Jas S. Kalsi, Herman S. Fernando, Iqbal S. Shergill, Asif Muneer, Hashim U. Ahmed, MCQs for the FRCS(Urol) and Postgraduate Urology Examinations, 2020
Nilay Patel (deceased), Vinodh Murali, David Cranston
When functional renal tissue is removed, glomerular hyperfiltration occurs in the remaining tissue to restore filtration capacity. Prolonged glomerular hyperfiltration may lead to renal injury in the form of focal segmental glomerulosclerosis and progressive renal failure [30].
The Diabetic/Obese Hypertensive Patient (Including Metabolic Syndrome)
Published in Giuseppe Mancia, Guido Grassi, Konstantinos P. Tsioufis, Anna F. Dominiczak, Enrico Agabiti Rosei, Manual of Hypertension of the European Society of Hypertension, 2019
Diabetes mellitus and hypertension are independent factors for chronic kidney disease (CKD). A large European cohort reported that obesity per se is also one of the strongest risk factors for new onset of CKD (47). Kidney impairment in obesity starts with glomerular hyperfiltration, which is observed before the appearance of glomerulomegaly or renal dysfunction; thus it could be considered an early marker of obesity-related kidney disease. The primary histologic features in obesity are relatively few lesions of focal-segmental glomerulosclerosis, profound glomerulomegaly due to glomerular hyalinosis and fibrosis, as well as lipid accumulation in the glomeruli and adhesion to Bowman’s capsule (16). Diabetic nephropathy starts with glomerular basement membrane thickening followed by mesangial expansion, nodular sclerosis and finally glomerulosclerosis. In clinical praxis diabetic nephropathy can be detected either as increased e-GFR or microalbuminuria in the early stages of the disease, followed by proteinuria that can reach the nephrotic syndrome values and reduction in e-GFR hypofiltration leading to end-stage renal disease (ESRD). Obesity, hypertension and diabetes are the most common causes of ESRD in Western countries (48).
Extending the ambit of SGLT2 inhibitors beyond diabetes: a review of clinical and preclinical studies on non-diabetic kidney disease
Published in Expert Review of Clinical Pharmacology, 2021
Saurabh Nayak, Vinay Rathore, Joyita Bharati, Kamal Kant Sahu
Importantly, the magnitude of benefit observed lacks a perfect correlation with the proposed nephroprotective mechanism of these agents, mainly glomerular hyperfiltration (GH) reduction. Rather, they are known to act on various lines to preserve kidney function, extending from reduction of GH through tubulo-glomerular feedback (TGF) activation and multiple pleiotropic effects on tubules. Nevertheless, encouraging results of Dapagliflozin in Patients with Chronic Kidney Disease (DAPA-CKD) trial that included one-third of non-diabetic CKD patients without heart failure have expanded the role of SGLT2i as a nephroprotective agent beyond the purview of diabetes mellitus. Ancillary analysis of the DAPA-CKD trial found consistent efficacy of Dapagliflozin among patients with diabetic nephropathy, various glomerulonephritis, ischemic or hypertensive CKD, and CKD of unknown cause [8]. In this review, we discuss various preclinical and clinical studies that address possible mechanisms of nephroprotection offered by SGLT2i in states of non-diabetic CKD.
Smoking tobacco is associated with renal hyperfiltration
Published in Scandinavian Journal of Clinical and Laboratory Investigation, 2021
Malin Mickelsson, Elisabet Söderström, Kristina Stefansson, Jonas Andersson, Stefan Söderberg, Johan Hultdin
To our knowledge, all previous studies on the consumption of tobacco reporting an increased eGFR only evaluated eGFRcreatinine and not eGFRcystatin C [11–15] or used measured mGFR based on cr-EDTA clearance [21]. In our study, we evaluated both eGFRcreatinine and eGFRcystatin C. One study reported a decreased GFR and a higher risk for renal function decline based on MAG3-clearance but not for mGFR based on DTPA-clearance [7]. Other studies measured urinary albumin excretion [9], or when using eGFR, followed the participants for five to ten years until developing CKD [6,8], thus possibly missing the early phase of renal disease. Renal hyperfiltration might be a marker of early glomerular damage, supported by a recent systematic review suggesting that 'glomerular hyperfiltration is thought to play an important role in the initiation of glomerular damage’ [32]. Renal hyperfiltration has also been associated with increased cardiovascular risk, carotid plaques, rapid decline in renal function in people with diabetes, obesity and other metabolic parameters [16–20].
Longer time spent in bed attempting to sleep is associated with rapid renal function decline: the Dongfeng–Tongji cohort study
Published in Annals of Medicine, 2018
Yizhun Li, Liangle Yang, Hao Wang, Haijing Jiang, Gaokun Qiu, Yiyi Liu, Yang Xiao, Handong Yang, Tangchun Wu, Xiaomin Zhang
Abnormal sleep duration has been suggested to be associated with adverse health outcomes [8,9]. Several cross-sectional studies showed that short or long sleep duration was associated with renal parameters or prevalent CKD [10–13]. However, prospective evidence on such relation was limited. Two prospective cohort studies in the US and one retrospective cohort study in Japan found that shorter sleep duration was independently associated with the higher estimated glomerular filtration rate (eGFR), rapid decline in renal function and development of proteinuria, respectively [14–16]. Actigraphy-estimated sleep duration, sleep duration per 24 h and self-reported categorical, habitual sleep duration were used in the three studies. To the best of our knowledge, little is known about the relationship between renal parameters and time in bed which was associated with blood pressure and self-reported myocardial infarction, stroke and cancer [17,18]. In addition, the definition of glomerular hyperfiltration varied in different studies and the prevalence rate of glomerular hyperfiltration among the elderly was unknown [19], therefore examining it in the population might be unjustified, then we focused on rapid renal function decline, which was commonly used as an outcome in prospective studies [20,21]. Therefore, in the present study, we aimed to investigate the association of time spent in bed attempting to sleep (TSBS) with rapid renal function decline in a middle-aged and elderly Chinese adults from the Dongfeng–Tongi (DFTJ) cohort, and whether the association could be modified by different characteristics or disease status.