Hyperchloremic Metabolic Acidosis: Renal Tubular Acidosis

2013 ◽  
pp. 347-370
Author(s):  
Alluru S. Reddi
Keyword(s):  
Metabolic Acidosis ◽  
Renal Tubular Acidosis ◽  
Hyperchloremic Metabolic Acidosis ◽  
Renal Tubular

scholarly journals Clinical approach to renal tubular acidosis in children

2021 ◽  
Vol 35 ◽  
pp. 88-94
Author(s):  
Soumya Reddy ◽  
Nivedita Kamath
Keyword(s):  
Metabolic Disease ◽  
Metabolic Acidosis ◽  
Renal Tubular Acidosis ◽  
Fanconi Syndrome ◽  
Specific Treatment ◽  
Supportive Therapy ◽  
Distal Tubule ◽  
Clinical Approach ◽  
Hyperchloremic Metabolic Acidosis ◽  
Renal Tubular

Renal tubular acidosis (RTA) is a common inherited tubulopathy in children. Proximal RTA, usually secondary to a systemic metabolic disease, is characterized by a generalized dysfunction of the proximal tubule resulting in Fanconi syndrome. Distal RTA occurs due to mutation in the transporters of the distal tubule resulting in acidification defects. Hyperchloremic metabolic acidosis with normal anion gap is the characteristic feature of RTA. In addition to supportive therapy, specific treatment for the underlying etiology and regular monitoring of growth and laboratory parameters are of utmost importance.

P0002A NEW INSIGHT INTO THE MECHANISM OF HYPERCHLOREMIC METABOLIC ACIDOSIS IN KIDNEY TRANSPLANT RECIPIENTS: INCREASED POSTGLOMERULAR PERITUBULAR BLOOD FLOW IS A KEY CONDITION FOR THE DEVELOPEMENT OF CALCINEURIN INHIBITOR-INDUCED RENAL TUBULAR ACIDOSIS

2020 ◽  
Vol 35 (Supplement_3) ◽  
Author(s):  
Shuzo Kaneko ◽  
Joichi Usui ◽  
Kazuhiro Takahashi ◽  
Tomokazu Kimura ◽  
Akio Hoshi ◽  
...  
Keyword(s):  
Blood Flow ◽  
Metabolic Acidosis ◽  
Kidney Transplant ◽  
Renal Tubular Acidosis ◽  
Trough Level ◽  
Transplant Recipients ◽  
Kidney Transplant Recipients ◽  
Renal Hemodynamic ◽  
Hyperchloremic Metabolic Acidosis ◽  
Renal Tubular

Abstract Background and Aims Hyperchloremic metabolic acidosis (HCMA) due to renal tubular acidosis is a common complication in kidney transplant recipients(KTR). Potential renal dysfunction, rejection, ischemia, persistent hyperparathyroidism, calcineurin inhibitors (CNIs), etc. have been identified as causes but have not been fully proven, and whether HCMA is a determinant of poor graft prognosis in KTR is still controversial. The purpose of this study is to elucidate the actual mechanism of HCMA in KTR. Method HCMA was defined as follows: i) simple strong ion difference (SID) Na-CL, which is the most dominant metabolic factor in physicochemical approach for acid-base balance, is 34 or less, or â…±) the alkalizing drugs have been started after the KT to correct HCMA. And all the cases of having diarrhea from mycophenolate mofetil(MMF), and gastroenterocolitis from cytomegalovirus infection were excluded. The study group consisted of 47 KTRs who underwent living-kidney transplantation(KT) at our hospital as well as a control group of 43 of the matched donors. Among them, a total of 26 KTRs received the renal hemodynamic studies which were based on urinary clearance of inulin and para-aminohippuric acid 1year after KT. 1) The incidence of HCMA in KTR at 3 months(3m) and 1 year(1y) after KT were examined. 2) To elucidate factors related to HCMA in KTR at 1y, we comprehensively examined factors and compared HCMA groups with non-HCMA groups; donor and recipient background (gender, age, body size), immunological factors, information on transplant surgery, salt and protein intake, effective buffering factors for extracellular body fluids such as albumin and hemoglobin, serum calcium and phosphate concentrations and their ratios, administration of renin-angiotensin system inhibitors and diuretics,Tac trough level and Banff score of each histopathological lesion in 1y biopsy. As for the 26 KTRs who received the renal hemodynamic studies, glomerular filtration rate (GFR), renal plasma flow (RPF), filtration fraction(FF) (GFR/RPF) and pre-/post-glomerular vascular resistance (pre-/postVR) calculated from the Gomez' equations were also analyzed. Results 1) The incidence of HCMA in the KTR at 3m was 51% (24/47), which was much higher than the 6.9% (3/43) in those donors (p<0.001), and the range of odds ratios (vs donor) adjusted by the background factors (age,gender, estimated GFR, albumin and hemoglobin) was 6.7-15.7 (p=0.0001-0.001). The incidence of HCMA in KTR at 1y decreased to 34%. 2)The univariate analysis of HCMA in KTR at 1y compared with non-HCMA showed an increase in RPF (p= 0.016), a decrease in post-VR (p= 0.003), and a decrease in FF (p= 0.0001), suggesting an increase in post-glomerular peritubular blood flow. In addition, the aah lesion score, an indicator of CNI vasculopathy, was also significantly higher in the HCMA (p = 0.015). There was no difference in Tac trough levels between HCMA and nonHCMA, and no independent factors were found by multivariate analysis. All cases with HCMA were classified into low post-VR (Fig.1). Furthermore, in low post-VR alone (n= 15), the Tac trough level at 1y was significantly higher in the HCMA (p= 0.002) (Fig.2). Conclusion In kidney transplant recipients, increased post-glomerular peritubular blood flow is a key condition for the development of CNI-induced renal tubular acidosis. The presence of HCMA suggests that it is probably not a serious condition, but rather a desirable hemodynamic state, however, more attention should be paid not to elevate CNI concentration levels in such conditions.

scholarly journals Acute Respiratory Failure Due to Hypokalaemic Muscular Paralysis from Renal Tubular Acidosis

2005 ◽  
Vol 33 (5) ◽  
pp. 656-658 ◽  
Author(s):  
S. Gombar ◽  
P. J. Mathew ◽  
K. K. Gombar ◽  
S. D'Cruz ◽  
G. Goyal
Keyword(s):  
Mechanical Ventilation ◽  
Metabolic Acidosis ◽  
Respiratory Failure ◽  
Acute Respiratory Failure ◽  
Renal Tubular Acidosis ◽  
Cardiac Arrhythmias ◽  
Distal Renal Tubular Acidosis ◽  
Life Threatening ◽  
Renal Tubular ◽  
Potassium Replacement

We report a case of hypokalaemic quadriplegia with acute respiratory failure and life-threatening cardiac arrhythmias in a 26-year-old woman who was diagnosed to have distal renal tubular acidosis. She had persistent metabolic acidosis with severe hypokalaemia and required mechanical ventilation and potassium replacement. The anaesthetic implications of renal tubular acidosis are also discussed.

scholarly journals Metabolic acidosis in toluene sniffing

CJEM ◽  
2013 ◽  
Vol 15 (04) ◽  
pp. 249-252 ◽  
Author(s):  
Jon Tuchscherer ◽  
Habib Rehman
Keyword(s):  
Metabolic Acidosis ◽  
Renal Tubular Acidosis ◽  
Excretion Rate ◽  
Ammonia Excretion ◽  
Distal Renal Tubular Acidosis ◽  
Anion Gap ◽  
Renal Tubular ◽  
Conjugate Bases ◽  
Osmolal Gap ◽  
Ammonia Excretion Rate

ABSTRACT Toluene sniffing, frequently described under the generic category of “glue sniffing,” is a potential cause of normal anion gap metabolic acidosis due to distal renal tubular acidosis. Urine anion gap is used to diagnose metabolic acidosis of a normal anion gap variety; however, pitfalls exist when using urine anion gap in the setting of toluene sniffing. We present the case of a young woman who had a normal anion gap metabolic acidosis due to toluene sniffing and an unexpectedly low urine anion gap. In such a scenario, the urine anion gap will underestimate the rate of ammonia excretion when the conjugate bases of acids other than HCl are excreted in large quantities. Estimation of the urine osmolal gap will provide a more accurate ammonia excretion rate in these circumstances. The challenges in interpretation of the urine anion gap and ammonia excretion in the setting of distal renal tubular acidosis due to toluene toxicity are discussed.

scholarly journals SUN-185 Severe Hyponatremia and Type 4 Renal Tubular Acidosis (Functional Hypoaldosteronism) Secondary to Trimethoprim

2020 ◽  
Vol 4 (Supplement_1) ◽  
Author(s):  
Yun Qing Koh ◽  
Kian Ming Jeremy Hoe ◽  
Timothy Peng Lim Quek
Keyword(s):  
Metabolic Acidosis ◽  
Sodium Chloride ◽  
Sodium Bicarbonate ◽  
Renal Tubular Acidosis ◽  
Anion Gap ◽  
Aortic Graft ◽  
Acid Base ◽  
Severe Hyponatremia ◽  
Renal Tubular ◽  
Oral Sodium

Abstract Introduction: Trimethoprim-sulfamethoxazole (TMP-SMX) is a commonly used antibiotic. We present a case of severe hyponatremia and Type 4 renal tubular acidosis (functional hypoaldosteronism) in a patient treated with TMP-SMX. Clinical Case: A 62 year old gentleman with hypertension, dyslipidemia and a surgically repaired abdominal aortic aneurysm developed an aortic graft infection. He was admitted to hospital for acute right lower limb ischemia with embolic phenomena, and underwent surgical graft explantation. He required multiple courses of antibiotics post operatively. He was initially referred to Endocrinology for severe hyponatremia, deemed likely to be from a salt losing nephropathy secondary to polymyxin. Thyroid function and morning cortisol levels were normal. He was managed with intravenous hypertonic saline and oral salt tablets. The hyponatraemia resolved a week after polymyxin was stopped. Intravenous TMP-SMX was commenced the next day at 240 mg BD. A week later, the hyponatremia recurred, with concomitant hyperkalemia and a normal anion gap metabolic acidosis. The serum sodium was 126 mmol/L (reference interval (RI) 135-145) and the serum osmolality 275 mmol/kg (RI 275- 305). Urine studies showed a high urinary sodium (154 mmol/L) and osmolality (481 mmol/kg), consistent with renal salt wasting. The serum potassium rose to a peak of 6.1 mmol/L (RI 3.5 - 5.0), with a normal anion gap metabolic acidosis (bicarbonate 17 mmol/L (RI 21 – 31)). A paired urine pH of 8 pointed to an inability to acidify the urine. Given the clinical course and laboratory investigations, the diagnosis of TMP-associated hyponatremia and Type 4 RTA was made. Oral resonium was started to correct hyperkalemia, with a combination of oral sodium chloride and sodium bicarbonate used to treat the hyponatremia and metabolic acidosis. Fludrocortisone was not used given the concerns of causing hypertension in a patient with a diseased aortic graft. The dose of TMP-SMX was gradually reduced with improvement of the acid-base and electrolyte abnormalities, lending weight to our diagnosis. After the dose of the TMP-SMX was reduced to 80 mg BD, the hyperkalemia and metabolic acidosis resolved. The oral sodium chloride and sodium bicarbonate were gradually tailed off and stopped after cessation of the TMP-SMX. Clinical Lesson: Trimethoprim blocks the epithelial sodium channel (ENaC) of the principal cells in the terminal portion of the nephron, similar to potassium sparing diuretics like amiloride and triampterene. The resulting hyponatremia, hyperkalemia and metabolic acidosis can be life threatening. Therefore, monitoring of electrolytes and acid base status is important, particularly in susceptible patients or in those where a high dose of trimethoprim is required.

scholarly journals ASIDOSIS TUBULAR RENAL DISTAL

2020 ◽  
Vol 5 (1) ◽  
pp. 265
Author(s):  
Ayu Pathya ◽  
Harnavi Harun
Keyword(s):  
Metabolic Acidosis ◽  
Renal Tubular Acidosis ◽  
Bone Growth ◽  
Hydrogen Ion ◽  
Genetic Mutations ◽  
Growth Disorders ◽  
Urine Ph ◽  
Renal Tubular ◽  
Hands And Feet

<p><em>Asidosis tubular renal (ATR) merupakan tubulopati ginjal yang jarang terjadi, dimana terdapat ketidakmampuan ginjal untuk menjaga perbedaan pH normal antara darah dan lumen tubulus ginjal. Pada kondisi ini terjadi gangguan pengasaman urin disebabkan gangguan reabsorbsi bikarbonat, gangguan ekskresi ion hidrogen, atau keduanya sehingga mengakibatkan asidosis metabolik. ATR ditandai dengan adanya asidosis metabolik dengan senjang anion plasma yang normal, hiperkloremik dan laju filtrasi glomerulus normal. ATR terbagi menjadi 3 tipe utama, yaitu ATR tipe 1 (ATR distal), tipe-2 (ATR proksimal), dan tipe 4 (ATR hiperkalemia). ATR distal merupakan ATR yang disebabkan oleh defek pada tubulus distal ginjal, dimana defek ini menyebabkan gangguan pada sekresi ion hidrogen. Beberapa penelitian menunjukkan bahwa ATR tipe 1 dikaitkan dengan mutasi genetik. Mutasi genetik herediter dapat autosomal dominan atau autosomal resesif. Gambaran klinis dapat mencakup kelainan pertumbuhan tulang, kelemahan atau kelumpuhan otot, deposit kalsium di ginjal, anoreksia, muntah, konstipasi, diare, dehidrasi, dan poliuria. Telah dilaporkan kasus pasien wanita usia 19 tahun dengan keluhan utama kelemahan di kedua tangan dan kaki. Dari penelusuran klinis dan laboratorium  didapatkan hipokalemia dan berdasarkan pendekatan hipokalemia dengan HCO3- rendah dan pH urine &gt;5,5, diagnosis pada pasien ini ditegakkan sebagai asidosis tubulus renal distal (ATRd).</em></p><p><strong><em>Kata kunci:</em></strong><em> </em><em>ATR, ATRd,  asidosis metabolik, hiperkloremik, hipokalemia </em><em></em></p><p><strong><em>Abstract</em></strong></p><p><em>Renal tubular acidosis (RTA) is a condition caused by the inability of the kidneys to maintain normal pH differences between the blood and tubules lumen of the kidney. Renal tubular acidosis is a rare kidney tubulopathy. In this condition, urine acidification is caused by bicarbonate reabsorption, disruption of hydrogen ion excretion, or both, resulting in metabolic acidosis. RTA is characterized by metabolic acidosis with normal plasma anion, hyperchloremic gaps and normal glomerular filtration rates. RTA is divided into 3 main types, namely type 1 RTA (distal RTA), type-2 (proximal RTA), and type 4 (hyperkalemia RTA). Distal RTA caused by defects in the distal tubules of the kidney, where these defects cause interference with the hydrogen ion secretion. Several studies have shown that type 1 RTA is associated with genetic mutations. Hereditary genetic mutations can be autosomal dominant or autosomal recessive. Clinical features can include bone growth disorders, muscle weakness or paralysis, calcium deposits in the kidneys, anorexia, vomiting, constipation, diarrhea, dehydration, and polyuria. There has been a reported case of a 19-year-old female patient with a chief complaint weakness in both hands and feet. From clinical and laboratory investigations, it was found that hypopotassium and based on the hypokalemia approach with low HCO3- and urine pH &gt;5,5, the diagnosis in this patient was established as a distal renal tubular acidosis (RTAd)</em> <strong><em> </em></strong></p><p><strong><em>Keywords: </em></strong><em>RTA, RTAd ,metabolic acidosis, hypopotassium, hiperchloremic</em></p><p><em> </em></p>

Glue-sniffing and distal renal tubular acidosis: sticking to the facts.

1991 ◽  
Vol 1 (8) ◽  
pp. 1019-1027 ◽  
Author(s):  
E J Carlisle ◽  
S M Donnelly ◽  
S Vasuvattakul ◽  
K S Kamel ◽  
S Tobe ◽  
...  
Keyword(s):  
Metabolic Acidosis ◽  
Renal Tubular Acidosis ◽  
Extracellular Fluid ◽  
Distal Renal Tubular Acidosis ◽  
Anion Gap ◽  
Acid Base ◽  
Major Question ◽  
The Subject ◽  
Renal Tubular ◽  
Sodium And Potassium

An index case is presented to introduce the subject of the acid-base and electrolyte abnormalities resulting from toluene abuse. These include metabolic acidosis associated with a normal anion gap and excessive loss of sodium and potassium in the urine. The major question addressed is, what is the basis for the metabolic acidosis? Overproduction of hippuric acid resulting from the metabolism of toluene plays a more important role in the genesis of the metabolic acidosis than was previously believed. This conclusion is supported by the observation that the rate of excretion of ammonium was not low during metabolic acidosis in six of eight patients, suggesting that distal renal tubular acidosis was not an important acid-base abnormality in most cases where ammonium was measured. The excretion of hippurate in the urine unmatched by ammonium also mandates an enhanced rate of excretion of the cations, sodium and potassium. The loss of sodium causes extracellular fluid volume contraction and a fall in the glomerular filtration rate, which may transform the normal anion gap type of metabolic acidosis into one with a high anion gap (accumulation of hippurate and other anions). Continuing loss of potassium in the urine leads to hypokalemia. An understanding of the metabolism of toluene provides the basis for the unusual biochemical abnormalities seen with abuse of this solvent.

Complex Acid-Base Disorders in Subacute Necrotizing Encephalomyelopathy (Leigh's Syndrome)

PEDIATRICS ◽  
1978 ◽  
Vol 61 (2) ◽  
pp. 278-281
Author(s):  
Gladys H. Hirschman ◽  
James C. M. Chan
Keyword(s):  
Metabolic Acidosis ◽  
Clinical Data ◽  
Renal Tubular Acidosis ◽  
Respiratory Alkalosis ◽  
Type I ◽  
Type Ii ◽  
Acid Base ◽  
Hybrid Type ◽  
Leigh’S Syndrome ◽  
Renal Tubular

This report describes a case of subacute necrotizing encephalomyelopathy (Leigh's syndrome) in a 7-month-old boy. The clinical data suggest an association with a disorder of renal tubular acidification, characterized by both (proximal) type II and (distal) type I renal tubular acidosis (hybrid type). Concomitantly, the initial uncompensated metabolic acidosis evolved into a mixed metabolic acidosis and respiratory alkalosis-features of this syndrome not previously reported.

Sign in / Sign up

Export Citation Format

Share Document