A Short Duration Renal Acidification Test Using Calcium Chloride

Oster, James R.; Hotchkiss, Jeanne L.; Carbon, Michael; Farmer, Marcella; Vaamonde, Carlos A.

doi:10.1159/000180458

Cited by 42 publications

(12 citation statements)

References 10 publications

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“…Another important concern is about how the follow-up after the CaCl 2 loading test was performed. The original report of CaCl 2 test followed patients for up to 6 h [17]. Due to technical issues, we only followed the patients for 4 h. It is possible that some patients could have had a normal urinary acidification test after 4 h of CaCl 2 administration, but this does not invalidate our findings.…”

Section: Discussionmentioning

confidence: 97%

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Renal Function Improvement with Pentavalent Antimonial Agents in Patients with Visceral Leishmaniasis

Daher

Rocha²,

Oliveira

et al. 2011

Am J Nephrol

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Background: The aim of this study is to investigate tubular and glomerular function after visceral leishmaniasis (VL) treatment with pentavalent antimonials. Methods: This is a prospective study including 14 patients with VL diagnosis treated with pentavalent antimonials. Urine acidification and concentration tests were performed. Estimated glomerular filtration rate (eGFR), fractional excretion of sodium (FE_Na) and potassium (FE_K) and free water clearance (C_H2O) were measured to assess glomerular and tubular function. Results: The VL group had a significantly lower FE_K, serum sodium and plasma osmolality (P_osm). No significant differences were found regarding proteinuria, eGFR, FE_Na or C_H2O. Patients in the VL group had lower urinary osmolality (U_osm) before DDAVP use when compared to the control group, as well as a lower U/P_osm. The urinary pH before and after CaCl₂ load was higher in the VL group. Conclusion: This study shows evidence of reversal of some tubular dysfunction in VL, but other dysfunctions may persist, especially urinary acidification capacity.

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Section: Discussionmentioning

confidence: 97%

“…The U/P osm ratio was calculated and a value less than 2.8 was considered abnormal. Urinary acidification was evaluated by measuring urinary pH (U pH ) at baseline (T₀) and 4 h after ingestion of CaCl 2 (T 4 ), 2 mEq/kg of body weight [17]. All tubular function tests were also performed in the control group.…”

Section: Methodsmentioning

confidence: 99%

Renal Function Improvement with Pentavalent Antimonial Agents in Patients with Visceral Leishmaniasis

Daher

Rocha²,

Oliveira

et al. 2011

Am J Nephrol

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“…Although it is well established that some acidoses result in the liberation of phosphorus from organic com pounds within cells [17 ,18], these studies have not included acute observations and have not evaluated the effects of several physiologically important acidifying agents. In this regard, exaggerated hyperphosphatemia was described recently in patients with lactic acidosis [19], and normal or slightly elevated levels have been reported in patients with diabetic ketoacidosis [20], while other data suggest that NH iCI-induced acidosis is not associated with increases in plasma phosphorus [7,21].…”

Section: Experimental Studiesmentioning

confidence: 90%

Serum Potassium Concentration in Acidemic States

Pérez¹,

Oster²,

Vaamonde³

1981

Nephron

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It has been generally accepted that acidosis results in hyperkalemia because of shifts of potassium from the intracellular to the extracellular compartment. There is ample clinical and experimental evidence, however, to support the conclusion that uncomplicated organic acidemias do not produce hyperkalemia. In acidosis associated with mineral acids (respiratory acidosis, end-stage uremic acidosis, NH₄CI- or CaCl₂-induced acidosis), acidemia per se, results in predictable increases in serum potassium concentration. In acidosis associated with nonmineral organic acids (diabetic and alcoholic acidosis, lactic acidosis, methanol and the less common forms of organic acidemias secondary to methylmalonic and isovaleric acids, and ethylene glycol, paraldehyde and salicylate intoxications), serum potassium concentration usually remains within the normal range in uncomplicated cases. A number of factors, however, may be responsible for hyperkalemia in some of these patients other than the acidemia per se. These include dehydration and renal hypoperfusion, preexisting renal disease, hypercatabolism, diabetes mellitus, hypoaldosteronism, the status of potassium balance, and therapy. The mechanism(s) of this differing effect of mineral and organic acidemias on transmembrane movement of potassium remains undefined. The prevalent hypothesis, however, favors the free penetrance of the organic anion into cells without creating a gradient for the hydrogen ions and, thus, obviating the efflux of intracellular potassium. The importance of the presence of hyperkalemia in clinical states of organic acidemias is obvious. A search for the complicating factors reviewed above should be undertaken since organic acidemias per se, should not be expected to be accompanied by elevations of serum potassium concentration. Moreover, the classical teaching that the absence of hyperkalemia during severe acidosis is indicative of severe potassium deficiency, may not be universally valid in patients with uncomplicated organic acidemias.

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“…Urinary concentration ability was evaluated through the ratio between urinary and serum osmolality (U osm /P osm ) after 12 hours water deprivation. Urinary acidification was evaluated through the measure of urinary pH before and after administration of oral CaCl 2 2mEq/kg (T₀ and T 4 ), as it is more tolerable than ammonium chloride [7]. Acidification defect was determined by the inability in decreasing U pH for less than 5.3 after the administration of the acid load, as described before [8].…”

Section: Methodsmentioning

confidence: 99%

Renal Tubular Dysfunction in Sickle Cell Disease

Silva

Vieira

Couto

et al. 2013

Kidney Blood Press Res

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Background/Aims: Kidney abnormalities are one of the main chronic complications of sickle cell disease (SCD). The aim of this study is to investigate the occurrence of renal tubular abnormalities among patients with SCD. Methods: This is a prospective study with 26 SCD adult patients in Brazil. Urinary acidification and concentration tests were performed using calcium chloride (CaCl₂), after a 12h period of water and food deprivation. Fractional excretion of sodium (FE_Na), transtubular potassium gradient (TTKG) and solute free water reabsorption (TcH₂O) were calculated. The SCD group was compared to a group of 15 healthy volunteers (control group). Results: Patient`s average age and gender were similar to controls. Urinary acidification deficit was found in 10 SCD patients (38.4%), who presented urinary pH >5.3 after CaCl₂ test. Urinary osmolality was significantly lower in SCD patients (355±60 vs. 818±202mOsm/kg, p=0.0001, after 12h period water deprivation). Urinary concentration deficit was found in all SCD patients (100%). FE_Na was higher among SCD patients (0.75±0.3 vs. 0.55±0.2%, p=0.02). The TTKG was higher in SCD patients (5.5±2.5 vs. 3.0±1.5, p=0.001), and TcH₂O was lower (0.22±0.3 vs. 1.1±0.3L/day, p=0.0001). Conclusions: SCD is associated with important kidney dysfunction. The main abnormalities found were urinary concentrating and incomplete distal acidification defect. There was also an increase in the potassium transport and decrease in water reabsorption, evidencing the occurrence of distal tubular dysfunction.

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A Short Duration Renal Acidification Test Using Calcium Chloride

Cited by 42 publications

References 10 publications

Renal Function Improvement with Pentavalent Antimonial Agents in Patients with Visceral Leishmaniasis

Renal Function Improvement with Pentavalent Antimonial Agents in Patients with Visceral Leishmaniasis

Serum Potassium Concentration in Acidemic States

Renal Tubular Dysfunction in Sickle Cell Disease

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