Renal Acid-Base Balance and Renal Tubular Acidosis

2007 ◽  
pp. 121-156
Author(s):  
Andrew I. Chin
Keyword(s):  
Renal Tubular Acidosis ◽  
Acid Base Balance ◽  
Acid Base ◽  
Base Balance ◽  
Renal Tubular

Complicated pregnancies in inherited distal renal tubular acidosis: importance of acid-base balance

2016 ◽  
Vol 30 (3) ◽  
pp. 455-460 ◽  
Author(s):  
Harald Seeger ◽  
Peter Salfeld ◽  
Rüdiger Eisel ◽  
Carsten A. Wagner ◽  
Nilufar Mohebbi
Keyword(s):  
Renal Tubular Acidosis ◽  
Distal Renal Tubular Acidosis ◽  
Acid Base Balance ◽  
Acid Base ◽  
Base Balance ◽  
Renal Tubular

scholarly journals Roles of Renal Proximal Tubule Transport in Acid/Base Balance and Blood Pressure Regulation

2014 ◽  
Vol 2014 ◽  
pp. 1-7 ◽  
Author(s):  
Motonobu Nakamura ◽  
Ayumi Shirai ◽  
Osamu Yamazaki ◽  
Nobuhiko Satoh ◽  
Masashi Suzuki ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Ang Ii ◽  
Acid Base Balance ◽  
Acid Base ◽  
Blood Pressure Homeostasis ◽  
Base Balance ◽  
Proximal Renal Tubular Acidosis ◽  
Renal Tubular ◽  
Regulation Of Blood Pressure

Sodium-coupled bicarbonate absorption from renal proximal tubules (PTs) plays a pivotal role in the maintenance of systemic acid/base balance. Indeed, mutations in the Na+-HCO3-cotransporter NBCe1, which mediates a majority of bicarbonate exit from PTs, cause severe proximal renal tubular acidosis associated with ocular and other extrarenal abnormalities. Sodium transport in PTs also plays an important role in the regulation of blood pressure. For example, PT transport stimulation by insulin may be involved in the pathogenesis of hypertension associated with insulin resistance. Type 1 angiotensin (Ang) II receptors in PT are critical for blood pressure homeostasis. Paradoxically, the effects of Ang II on PT transport are known to be biphasic. Unlike in other species, however, Ang II is recently shown to dose-dependently stimulate human PT transport via nitric oxide/cGMP/ERK pathway, which may represent a novel therapeutic target in human hypertension. In this paper, we will review the physiological and pathophysiological roles of PT transport.

Renal Tubular Acidosis in Children Treated With Trimethoprim-Sulfamethoxazole During Therapy for Acute Lymphoid Leukemia

PEDIATRICS ◽  
1992 ◽  
Vol 89 (6) ◽  
pp. 1072-1074
Author(s):  
Jerome Linus Murphy
Keyword(s):  
Renal Tubular Acidosis ◽  
Elevated Serum ◽  
Growth Failure ◽  
Serum Bicarbonate ◽  
Acid Base Balance ◽  
Urine Ph ◽  
Lymphoid Leukemia ◽  
Acute Lymphoid Leukemia ◽  
Base Balance ◽  
Renal Tubular

The antibiotics trimethoprim (TMP) and sulfamethoxazole (SMZ), when used in combination, can cause metabolic acidosis, renal bicarbonate wasting, and growth failure. Retrospective review of repeated random serum chemistries from 10 children receiving TMP-SMZ and maintenance chemotherapy for acute lymphoid leukemia revealed low serum bicarbonate (P = .0002) and elevated serum chloride (P < .0005) concentrations. These values normalized after all medications were discontinued. Prospective study of 8 children receiving TMP-SMZ and chemotherapy for acute lymphoid leukemia revealed lower serum bicarbonate concentrations and higher urine pH following a dose of TMP-SMZ than paired values obtained more than 3 days after a dose. Four children (50%) met serum bicarbonate and urinary pH criteria for the diagnosis of renal tubular acidosis soon after a dose of TMP-SMZ. The occurrence of TMP-SMZ-induced renal tubular acidosis has implications for the acid-base balance of children receiving TMP-SMZ on a long-term basis.

Two classic papers in acid-base physiology: contributions of R. F. Pitts, R. S. Alexander, and W. D. Lotspeich

2004 ◽  
Vol 287 (5) ◽  
pp. F864-F865 ◽  
Author(s):  
Gerhard Giebisch
Keyword(s):  
Acid Base Balance ◽  
Acid Base ◽  
Historical Significance ◽  
Base Balance ◽  
Renal Tubular ◽  
Classic Papers

This essay looks at the historical significance of two APS classic papers that are freely available online: Pitts RF and Alexander RS. The nature of the renal tubular mechanism for acidifying the urine. Am J Physiol 144: 239—254, 1945 ( http://ajplegacy.physiology.org/cgi/reprint/144/2/239 ). Pitts RF and Lotspeich WD. Bicarbonate and the renal regulation of acid base balance. Am J Physiol 147: 138—154, 1946 ( http://ajplegacy.physiology.org/cgi/reprint/147/1/138 ).

scholarly journals Disturbance of acid-base balance in cadmium-induced renal tubular dysfunction.

Sangyo Igaku ◽  
1990 ◽  
Vol 32 (4) ◽  
pp. 270-271
Author(s):  
Keiko AOSHIMA ◽  
Kokichi IWATA ◽  
Minoru KASUYA
Keyword(s):  
Tubular Dysfunction ◽  
Renal Tubular Dysfunction ◽  
Acid Base Balance ◽  
Acid Base ◽  
Base Balance ◽  
Renal Tubular

Acid-Base Disorders

2018 ◽  
Author(s):  
Aaron Skolnik ◽  
Jessica Monas
Keyword(s):  
Metabolic Acidosis ◽  
Renal Tubular Acidosis ◽  
Metabolic Alkalosis ◽  
Respiratory Acidosis ◽  
The Body ◽  
Anion Gap ◽  
Hydrogen Ions ◽  
Acid Base Balance ◽  
Acid Base ◽  
Renal Tubular

Under physiologic conditions, the acid-base balance of the body is maintained via changes in ventilation that eliminate carbon dioxide, buffering of acid loads, and renal excretion of hydrogen ions. Failure to maintain the pH of the blood between 7.35 and 7.45 can result in life-threatening conditions. This review details the pathophysiology, stabilization and assessment, diagnosis and treatment, and disposition and outcomes of acid-base disorders. Figures show the relationship between hydrogen ions and blood pH, proximal tubular bicarbonate reabsorption, the secretion of hydrogen ions, renal ammonia production, ammonium diffusion, metabolic alkalosis, electrocardiographic changes in hypokalemia and hyperkalemia, pseudoinfarction caused by hyperkalemia, and an algorithmic approach to suspected acid-base disorders. Tables list causes of high–anion gap metabolic acidosis, metabolic acidosis with a normal anion gap, type 1 renal tubular acidosis, type 4 renal tubular acidosis and aldosterone resistance, metabolic alkalosis, respiratory acidosis, and respiratory alkalosis; treatment of hyperkalemia; and a stepwise approach for the evaluation of suspected acid-base disorders. This review contains 9 highly rendered figures, 9 tables, 64 references, and a list of pertinent Web sites.

Acid-Base Disorders

2015 ◽  
Author(s):  
Aaron Skolnik ◽  
Jessica Monas
Keyword(s):  
Metabolic Acidosis ◽  
Renal Tubular Acidosis ◽  
Metabolic Alkalosis ◽  
Respiratory Acidosis ◽  
The Body ◽  
Anion Gap ◽  
Hydrogen Ions ◽  
Acid Base Balance ◽  
Acid Base ◽  
Renal Tubular

Under physiologic conditions, the acid-base balance of the body is maintained via changes in ventilation that eliminate carbon dioxide, buffering of acid loads, and renal excretion of hydrogen ions. Failure to maintain the pH of the blood between 7.35 and 7.45 can result in life-threatening conditions. This review details the pathophysiology, stabilization and assessment, diagnosis and treatment, and disposition and outcomes of acid-base disorders. Figures show the relationship between hydrogen ions and blood pH, proximal tubular bicarbonate reabsorption, the secretion of hydrogen ions, renal ammonia production, ammonium diffusion, metabolic alkalosis, electrocardiographic changes in hypokalemia and hyperkalemia, pseudoinfarction caused by hyperkalemia, and an algorithmic approach to suspected acid-base disorders. Tables list causes of high–anion gap metabolic acidosis, metabolic acidosis with a normal anion gap, type 1 renal tubular acidosis, type 4 renal tubular acidosis and aldosterone resistance, metabolic alkalosis, respiratory acidosis, and respiratory alkalosis; treatment of hyperkalemia; and a stepwise approach for the evaluation of suspected acid-base disorders. This review contains 9 highly rendered figures, 9 tables, 64 references, and a list of pertinent Web sites.

Higher Dietary Acidity is Associated with Lower Bone Mineral Density in Postmenopausal Iranian Women, Independent of Dietary Calcium Intake

2014 ◽  
Vol 84 (3-4) ◽  
pp. 0206-0217 ◽  
Author(s):  
Seyedeh-Elaheh Shariati-Bafghi ◽  
Elaheh Nosrat-Mirshekarlou ◽  
Mohsen Karamati ◽  
Bahram Rashidkhani
Keyword(s):  
Calcium Intake ◽  
Dietary Calcium ◽  
Dietary Calcium Intake ◽  
Dietary Intakes ◽  
Iranian Women ◽  
Acid Base Balance ◽  
Mineral Density ◽  
Acid Base ◽  
Base Balance ◽  
Dietary Acid

Findings of studies on the link between dietary acid-base balance and bone mass are relatively mixed. We examined the association between dietary acid-base balance and bone mineral density (BMD) in a sample of Iranian women, hypothesizing that a higher dietary acidity would be inversely associated with BMD, even when dietary calcium intake is adequate. In this cross-sectional study, lumbar spine and femoral neck BMDs of 151 postmenopausal women aged 50 - 85 years were measured using dual-energy x-ray absorptiometry. Dietary intakes were assessed using a validated food frequency questionnaire. Renal net acid excretion (RNAE), an estimate of acid-base balance, was then calculated indirectly from the diet using the formulae of Remer (based on dietary intakes of protein, phosphorus, potassium, and magnesium; RNAERemer) and Frassetto (based on dietary intakes of protein and potassium; RNAEFrassetto), and was energy adjusted by the residual method. After adjusting for potential confounders, multivariable adjusted means of the lumbar spine BMD of women in the highest tertiles of RNAERemer and RNAEFrassetto were significantly lower than those in the lowest tertiles (for RNAERemer: mean difference -0.084 g/cm2; P=0.007 and for RNAEFrassetto: mean difference - 0.088 g/cm2; P=0.004). Similar results were observed in a subgroup analysis of subjects with dietary calcium intake of >800 mg/day. In conclusion, a higher RNAE (i. e. more dietary acidity), which is associated with greater intake of acid-generating foods and lower intake of alkali-generating foods, may be involved in deteriorating the bone health of postmenopausal Iranian women, even in the context of adequate dietary calcium intake.

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