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1.
NSAIDs in CKD: Are They Safe?
Baker, M, Perazella, MA
American journal of kidney diseases : the official journal of the National Kidney Foundation. 2020;(4):546-557
Abstract
The management of pain in patients with chronic kidney disease (CKD) is challenging for many reasons. These patients have increased susceptibility to adverse drug effects due to altered drug metabolism and excretion, and there are limited safety data for use in this population despite a high pain burden. Nonsteroidal anti-inflammatory drugs (NSAIDs) have long been regarded as dangerous for use in patients with CKD because of their risk for nephrotoxicity and thus alternative classes of analgesics, including opioids, have become more commonly used for pain control in this population. Given the well-established risks that opioids and other analgesics pose, further characterization of the risk posed by NSAIDs in patients with CKD is warranted. NSAID use has been associated with acute kidney injury, progressive loss of glomerular filtration rate in CKD, electrolyte derangements, and hypervolemia with worsening of heart failure and hypertension. The risk for these nephrotoxicity syndromes is modified by many comorbid conditions, risk factors, and characteristics of use, and in patients with CKD, the risk differs between levels of glomerular filtration rate. In this review, we offer recommendations for the cautious use of NSAIDs in the CKD population after careful consideration of these risk factors on an individualized basis.
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2.
NAFLD as a driver of chronic kidney disease.
Byrne, CD, Targher, G
Journal of hepatology. 2020;(4):785-801
Abstract
Non-alcoholic fatty liver disease (NAFLD) and chronic kidney disease (CKD) are worldwide public health problems, affecting up to 25-30% (NAFLD), and up to 10-15% (CKD) of the general population. Recently, it has also been established that there is a strong association between NAFLD and CKD, regardless of the presence of potential confounding diseases such as obesity, hypertension and type 2 diabetes. Since NAFLD and CKD are both common diseases that often occur alongside other metabolic conditions, such as type 2 diabetes or metabolic syndrome, elucidating the relative impact of NAFLD on the risk of incident CKD presents a substantial challenge for investigators working in this research field. A growing body of epidemiological evidence suggests that NAFLD is an independent risk factor for CKD and recent evidence also suggests that associated factors such as metabolic syndrome, dysbiosis, unhealthy diets, platelet activation and processes associated with ageing could also contribute mechanisms linking NAFLD and CKD. This narrative review provides an overview of the literature on: a) the evidence for an association and causal link between NAFLD and CKD and b) the underlying mechanisms by which NAFLD (and factors strongly linked with NAFLD) may increase the risk of developing CKD.
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3.
[Bicarbonate: From physiology to treatment for all clinicians].
Beaume, J, Braconnier, A, Dolley-Hitze, T, Bertocchio, JP
Nephrologie & therapeutique. 2018;(1):13-23
Abstract
Acid-base regulation is essential to maintain homeostasis in humans. Carbonic acid/bicarbonate (H2CO3/HCO3-) couple is the most predominant extracellular buffer to keep plasma pH within a physiological range. The ability to (re)generate such a buffer is a key milestone that necessitates to understand a precise physiology of both renal tubule and digestive tract. Here, we first reviewed renal and digestive cycles of bicarbonate in physiology. We also reviewed pathological findings where acid-base disequilibrium is involved and nutritional and/or alkali therapy could be necessary. Secondly, data from clinical trials were synthesized. Alkali therapy, oral and parenteral, from mineral-based water, masterful preparations or pharmaceutics drugs, is regularly used in a wide range of clinical findings, even if supporting data are (often) of a low level of evidence. Bicarbonate is primarily used during contrast-induced nephropathy, metabolic acidosis in chronic kidney disease or nephrolithiasis in which alkaline urine is necessary. Cast nephropathy, rhabdomyolysis and tumor lysis syndrome make usually physicians prescribe alkali therapy even if this prescription is only supported by physiopathological data without any proven clinical results. Finally, bicarbonate is essential in the composition of dialysate in both hemodialysis and peritoneal dialysis.
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4.
Fatty Acids in Nephrotic Syndrome and Chronic Kidney Disease.
Turolo, S, Edefonti, A, Syren, ML, Marangoni, F, Morello, W, Agostoni, C, Montini, G
Journal of renal nutrition : the official journal of the Council on Renal Nutrition of the National Kidney Foundation. 2018;(3):145-155
Abstract
The role of fatty acids (FAs) in inflammation and in the related chronic diseases has been demonstrated. However, there is a lack of consistent and agreed knowledge about the role of FA profile and renal physiology and pathology, most articles focusing on the effect of polyunsaturated FAs supplementation, without considering the impact of basal FA metabolism on the efficacy of the supplementation. Here, we have summarized the specific literature concerning the assessment of circulating FA in 2 renal diseases, namely nephrotic syndrome and chronic kidney disease, also under hemodialytic treatment, and have received the most significant contributions in the last years. The effects of changes of FA profile and metabolism and the possible involvement of polyunsaturated FA metabolites in raising and modulating inflammation are discussed.
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5.
Evaluation of fracture risk in chronic kidney disease.
Torres, PAU, Cohen-Solal, M
Journal of nephrology. 2017;(5):653-661
Abstract
Chronic kidney disease (CKD) is associated with mineral and bone disorders (MBD) that are now considered as a syndrome. Bone fragility and a four to tenfold increased rate of skeletal fractures are often reported in CKD patients. The evaluation of the risk of these fractures in CKD patients should explore the same risk factors identified for the general population including low body weight, menopause, personal and familial history of osteoporosis, chronic inflammatory diseases, and corticosteroid therapy. The aim of this article is to provide a critical review of the tools used for the evaluation of bone loss and the risk of fracture in CKD patients, ranging from the measurement of bone mineral density (BMD), fracture risk assessment (Frax™), quantitative computed tomography (QCT), high-resolution peripheral quantitative computed tomography (HRpQTC), to circulating biomarkers of bone metabolism including vitamin D, parathyroid hormone (PTH), bone-specific alkaline phosphatase, osteocalcin, and some collagen type 1-related molecules indicators of bone remodeling.
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6.
The metabolic syndrome and chronic kidney disease.
Zhang, X, Lerman, LO
Translational research : the journal of laboratory and clinical medicine. 2017;:14-25
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Abstract
The metabolic syndrome (MetS) is a cluster of cardiovascular risk factors including insulin resistance (IR), dyslipidemia, and hypertension, which may also foster development of chronic kidney disease. The mechanisms of MetS-induced kidney disease are not fully understood. The purpose of this review is to summarize recent discoveries regarding the impact of MetS on the kidney, particularly on the renal microvasculature and cellular mitochondria. Fundamental manifestations of MetS include IR and adipose tissue expansion, the latter promoting chronic inflammation and oxidative stress that exacerbate IR. Those in turn can elicit various kidney injurious events through endothelial dysfunction, activation of the renin-angiotensin-aldosterone system, and adipokine imbalance. Inflammation and IR are also major contributors to microvascular remodeling and podocyte injury. Hence, these events may result in hypertension, albuminuria, and parenchymal damage. In addition, dyslipidemia and excessive nutrient availability may impair mitochondrial function and thereby promote progression of kidney cell damage. Elucidation of the link between MetS and kidney injury may help develop preventative measures and possibly novel therapeutic targets to alleviate and avert development of renal manifestations.
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7.
[The association of schizophrenia with chronic non transmissible diseases].
Orellana, G, Rodríguez, M, González, N, Durán, E
Revista medica de Chile. 2017;(8):1047-1053
Abstract
The life expectancy of patients with schizophrenia (SCH) is 11 to 20 years less than the general population. There is an association between SCH and various diseases and chronic conditions, highlighting the cardio-metabolic diseases. This association has been attributed to the use of antipsychotics, however, evidence has also shown intrinsic susceptibility of schizophrenic patients the development of chronic conditions. This review aims to update knowledge about chronic conditions such as cardiometabolic risk and sleep, bone and kidney disorders related to SCH. These patients have a high prevalence of risk behaviors, including smoking and poor diet. They have a worse metabolic profile than the general population and a greater likelihood of developing metabolic syndrome, diabetes and cardiovascular disease. SCH has also been associated with other chronic diseases such as osteoporosis and chronic kidney disease. The high prevalence of these comorbidities in schizophrenic population is not explained solely by the antipsychotic treatment, therefore intrinsic mechanisms associated to SCH are postulated to be associated with these conditions. This new information requires a change in the multidisciplinary medical approach for the study and management of schizophrenic patients.
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8.
Comorbidities in patients with crystal diseases and hyperuricemia.
Sattui, SE, Singh, JA, Gaffo, AL
Rheumatic diseases clinics of North America. 2014;(2):251-78
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Abstract
Crystal arthropathies are among the most common causes of painful inflammatory arthritis. Gout, the most common example, has been associated with cardiovascular and renal disease. In recent years, evidence for these associations and those involving other comorbidities, such as the metabolic syndrome, have emerged, and the importance of asymptomatic hyperuricemia has been established. In this review, an update on evidence, both experimental and clinical, is presented, and associations between hyperuricemia, gout, and several comorbidities are described. Causality regarding calcium pyrophosphate arthropathy and associated comorbidities is also reviewed.
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9.
Metabolic syndrome and associated chronic kidney diseases: nutritional interventions.
Kumar, PA, Chitra, PS, Reddy, GB
Reviews in endocrine & metabolic disorders. 2013;(3):273-86
Abstract
Lifestyle changes such as dietary habits, sedentary life and consumption of energy-dense foods that have occurred over the years has led to an epidemic of abdominal obesity, which in turn resulted in dramatic increase in the prevalence of metabolic syndrome (MetS). Different expert panels have provided various definitions for MetS to enable a clinical diagnosis and treatment of patients at risk of associated complications. Obesity and obesity mediated MetS has been paralleled by escalation in the incidence of chronic kidney disease (CKD). A better understanding of the pathophysiology of MetS and identification of individuals with MetS early in the life course could be important for initiating interventions such as lifestyle modification and dietary restrictions that form the basis for prevention and treatment of MetS and related co-morbidities including CKD. This review is intended to provide a comprehensive summary of the evolution of definition of MetS and association of MetS with CKD. In particular, mechanism of obesity and diabetes mediated CKD and emerging dietary therapies for MetS associated CKD will be discussed.
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10.
Renal dysfunction in methylmalonic acidurias: review for the pediatric nephrologist.
Morath, MA, Hörster, F, Sauer, SW
Pediatric nephrology (Berlin, Germany). 2013;(2):227-35
Abstract
Methylmalonic acidurias are a heterogeneous group of inborn errors of branched-chain amino acid metabolism. Depending on the underlying etiology, acute or chronic renal disease constitutes major (long-term) complications. In recent decades, overall survival has improved due to optimized treatment strategies based on the use of standardized emergency protocols and dialysis techniques. The majority of these patients, especially those having mut°, cblB, and cblA deficiency, are at increased risk of developing chronic kidney disease secondary to tubulointerstitial nephritis to require hemo- or peritoneal dialysis. Kidney and/or liver transplantation, as organ replacement, or even gene therapy on a limited scale, are controversially discussed treatment options in methylmalonic acidurias. The pathophysiological basis of renal disease has not been clarified in detail until now, but a severe mitochondrial dysfunction and an impairment of tubular dicarboxylic acid transport due to accumulated toxic metabolic compounds has been recently proposed. Another severe renal complication of methylmalonic acidurias is the occurrence of cblC-associated infantile atypical hemolytic syndrome, which can result in acute kidney injury. Close collaboration between (pediatric) nephrologists and metabolic specialists is required for the long-term management of these patients.