Urinary ammonia and long-term outcomes in chronic kidney disease

Vallet, Marion; Metzger, Marie; Haymann, Jean‐Philippe; Flamant, Martin; Gauci, Cédric; Thervet, Éric; Boffa, Jean‐Jacques; Vrtovsnik, François; Froissart, Marc; Stengel, Bénédicte; Houillier, Pascal

doi:10.1038/ki.2015.52

Cited by 125 publications

(132 citation statements)

References 34 publications

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“…The kidney is also endued with a large capacity to unload excess acid via ammonia (NH 3 ) genesis and (NH 4 + ) excretion. With declining kidney function, the capacity of bicarbonate conservation and generation decreases, while the net endogenous acid production in CKD remains unchanged, leading to the genesis of acidosis [38]. A reduced number of functioning nephrons in CKD also compromises the kidney's capacity to excrete excess acid (in the form of NH 4 + via ammonia genesis [38,39]).…”

Section: Metabolic Acidosismentioning

confidence: 99%

“…With declining kidney function, the capacity of bicarbonate conservation and generation decreases, while the net endogenous acid production in CKD remains unchanged, leading to the genesis of acidosis [38]. A reduced number of functioning nephrons in CKD also compromises the kidney's capacity to excrete excess acid (in the form of NH 4 + via ammonia genesis [38,39]). Notably, each residual-functioning nephron, however, undergoes hypertrophy and compensatorily generates a large amount of NH 3 [40,41].…”

Section: Metabolic Acidosismentioning

confidence: 99%

“…The consequent increase in the intra-renal NH 3 /NH 4 + can activate the complement pathway leading to tubulo-interstitial inflammation and injury [42]. Excess acid also increases endothelin-1 and aldosterone production [43,44], accelerating CKD progression [38,45,46,47]. …”

Section: Metabolic Acidosismentioning

confidence: 99%

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Electrolyte and Acid-Base Disorders in Chronic Kidney Disease and End-Stage Kidney Failure

Dhondup

Qian²

2017

Blood Purif

137

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The kidneys play a pivotal role in the regulation of electrolyte and acid-base balance. With progressive loss of kidney function, derangements in electrolytes and acid-base inevitably occur and contribute to poor patient outcomes. As chronic kidney disease (CKD) has become a worldwide epidemic, medical providers are increasingly confronted with such problems. Adequate diagnosis and treatment will minimize complications and can potentially be lifesaving. In this review, we discuss the current understanding of the disease process, clinical presentation, diagnosis and treatment strategies, integrating up-to-date knowledge in the field. Although electrolyte and acid-base derangements are significant causes of morbidity and mortality in CKD and end-stage renal disease patients, they can be effectively managed through a timely institution of combined preventive measures and pharmacological therapy. Exciting advances and several upcoming outcome trials will provide further information to guide treatment and improve patient outcomes.

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Section: Metabolic Acidosismentioning

confidence: 99%

Section: Metabolic Acidosismentioning

confidence: 99%

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Electrolyte and Acid-Base Disorders in Chronic Kidney Disease and End-Stage Kidney Failure

Dhondup

Qian²

2017

Blood Purif

137

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“…Indeed, metabolic acidosis in CKD is associated with more rapid CKD progression [30,31] and increased mortality [32] . Consistently maintaining normal ranges of serum HCO 3 -and correcting acidosis have been associated with favorable clinical outcomes [33][34][35][36][37][38] .…”

Section: Positive Acid Balancementioning

confidence: 99%

Inflammation: A Key Contributor to the Genesis and Progression of Chronic Kidney Disease

Qian

2017

Expanded Hemodialysis: Innovative Clinical Approach in Dialysis

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It has become apparent that inflammation and inflammatory reactions can evoke renal injury and promote chronic kidney disease (CKD) progression. Under physiological condition, intrarenal vascular distribution is heterogeneous, and medulla is hypoxic. To avoid energy deprivation in the low pO 2 regions of the kidney, an array of hormones, autocoids, and vasoactive substances, including medullipin, prostaglandins, endothelins, nitric oxide, angiotensin II, kinins, and adenosine, tonically regulates the microvasculature to ensure a perfect match of the microcirculation (O 2 supply) and renal tubules (O 2 demand). Inflammation, systemic or intrarenal, not only can abolish the microvascular response to its regulators, but also induces an array of tubular toxins, including reactive oxygen species, leading to tubular injury, nephron dropout, and onset of CKD. Positive acid balance, electrolyte alterations, and intestinal dysbiosis can perpetuate CKD progression. Understanding the role of inflammation in the genesis and progression of CKD will foster the development of strategies to prevent and treat the underlying inflammation and improve CKD outcomes.

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“…Eliichiro Kanda et al, study stated that patient with the lowest quartile of serum bicarbonate level show a high risk of chronic kidney disease progression compared with patients with high serum bicarbonate levels. [10][11][12][13][14][15] In present study group, many patients were in stage 4 and stage 5 have low serum bicarbonate level. Many patients in the study group had low serum bicarbonate level and only 07 patients were having high serum bicarbonate level who were in stage 3 and stage 4.…”

Section: No Of Patients 100%mentioning

confidence: 59%

Study of association of serum bicarbonate levels with mortality in chronic kidney disease

Kumar

Nikethan

2016

Int J Res Med Sci

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Urinary ammonia and long-term outcomes in chronic kidney disease

Cited by 125 publications

References 34 publications

Electrolyte and Acid-Base Disorders in Chronic Kidney Disease and End-Stage Kidney Failure

Electrolyte and Acid-Base Disorders in Chronic Kidney Disease and End-Stage Kidney Failure

Inflammation: A Key Contributor to the Genesis and Progression of Chronic Kidney Disease

Study of association of serum bicarbonate levels with mortality in chronic kidney disease

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