scholarly journals Transient pseudohypoaldosteronism

2011 ◽  
Vol 139 (1-2) ◽  
pp. 37-43
Author(s):  
Natasa Stajic ◽  
Jovana Putnik ◽  
Aleksandra Paripovic ◽  
Radovan Bogdanovic

Introduction. Infants with urinary tract malformations (UTM) presenting with urinary tract infection (UTI) are prone to develop transient type 1 pseudohypoaldosteronism (THPA1). Objective. Report on patient series with characteristics of THPA1, UTM and/or UTI and suggestions for the diagnosis and therapy. Methods. Patients underwent blood and urine electrolyte and acid-base analysis, serum aldosterosterone levels and plasma rennin activity measuring; urinalysis, urinoculture and renal ultrasound were done and medical and/or surgical therapy was instituted. Results. Hyponatraemia (120.9?5.8 mmol/L), hyperkalaemia (6.9?0.9 mmol/L), metabolic acidosis (plasma bicarbonate, 11?1.4 mmol/L), and a rise in serum creatinine levels (145?101 ?mol/L) were associated with inappropriately high urinary sodium (51.3?17.5 mmol/L) and low potassium (14.1?5.9 mmol/L) excretion. Elevated plasma aldosterone concentrations (170.4?100.5 ng/dL) and the very high levels of the plasma aldosterone to potassium ratio (25.2?15.6) together with diminished urinary K/Na values (0.31?0.19) indicated tubular resistance to aldosterone. After institution of appropriate medical and/or surgical therapy, serum electrolytes, creatinine, and acid-base balance were normalized. Imaging studies showed ureteropyelic or ureterovesical junction obstruction in 3 and 2 patients, respectively, posterior urethral valves in 3, and normal UT in 1 patient. According to our knowledge, this is the first report on THPA1 in the Serbian literature. Conclusion. Male infants with hyponatraemia, hyperkalaemia and metabolic acidosis have to have their urine examined and the renal ultrasound has to be done in order to avoid both, the underdiagnosis of THPA1 and the inappropriate medication.

1982 ◽  
Vol 242 (5) ◽  
pp. F544-F551 ◽  
Author(s):  
B. A. Stanton ◽  
G. Giebisch

To determine the relative importance of plasma and luminal pH changes as factors regulating potassium secretion by rat distal tubule, superficial tubules were continuously microperfused in vivo. The effects of changes in plasma pH were examined by producing acute systemic metabolic acidosis or alkalosis and holding luminal flow rate, solute composition, and pH constant by microperfusion. Alternatively, the effect of luminal solution pH was evaluated by microperfusing tubules with solutions buffered to either pH 6.5 or 8.0 at constant systemic acid-base balance. Net transport of Na and K and the pH of the luminal fluid were measured. Results showed that metabolic acidosis inhibited and metabolic alkalosis stimulated potassium secretion. Increased luminal fluid pH, in contrast, did not stimulate potassium transport. In experiments in which metabolic acidosis produced a diuresis, urinary potassium excretion was enhanced compared with hydropenic controls. Free-flow micropuncture studies revealed that the rate of fluid delivery to the distal tubule was 45% greater during acidosis compared with control and that potassium secretion increased in both the distal and collecting tubule. Since the rate of fluid delivery is a potent stimulus of potassium secretion in the distal tubule, it is concluded that the stimulus of increased delivery of fluid, observed in free-flow conditions, masked the inhibitory effect of acidosis on potassium transport. Potassium transport by the distal tubule, during acid-base disorders, is regulated by plasma pH and the rate of delivery of fluid but is not stimulated by alkalinization of the luminal fluid.


Author(s):  
Donaliazarti Donaliazarti ◽  
Rismawati Yaswir ◽  
Hanifah Maani ◽  
Efrida Efrida

Metabolic acidosis is prevalent among critically ill patients and the common cause of metabolic acidosis in ICU is lactic acidosis. However, not all ICUs can provide lactate measurement. The traditional method that uses Henderson-Hasselbach equation (completed with BE and AG) and alternative method consisting of Stewart and its modification (BDEgap and SIG), are acid-base balance parameters commonly used by clinicians to determine metabolic acidosis in critically ill patients. The objective of this study was to discover the association between acid-base parameters (BE, AGobserved, AGcalculated, SIG, BDEgap) with lactate level in critically ill patients with metabolic acidosis. This was an analytical study with a cross-sectional design. Eighty-four critically ill patients hospitalized in the ICU department Dr. M. Djamil Padang Hospital were recruited in this study from January to September 2016. Blood gas analysis and lactate measurement were performed by potentiometric and amperometric method while electrolytes and albumin measurement were done by ISE and colorimetric method (BCG). Linear regression analysis was used to evaluate the association between acid-base parameters with lactate level based on p-value less than 0.05. Fourty five (54%) were females and thirty-nine (46%) were males with participant’s ages ranged from 18 to 81 years old. Postoperative was the most reason for ICU admission (88%). Linear regression analysis showed that p-value for BE, AGobserved, AGcalculated, SIG and BDEgap were 119; 0.967; 0.001; 0.001; 0.689, respectively. Acid-base balance parameters which were mostly associated with lactate level in critically ill patients with metabolic acidosis were AGcalculated and SIG. 


1987 ◽  
Vol 253 (3) ◽  
pp. G330-G335
Author(s):  
D. S. Goldfarb ◽  
P. M. Ingrassia ◽  
A. N. Charney

We previously reported that systemic pH and HCO3 concentration affect ileal water and electrolyte absorption. To determine whether these effects could influence an ongoing secretory process, we measured transport in ileal loops exposed to either saline or 50-75 micrograms cholera toxin in mechanically ventilated Sprague-Dawley rats anesthetized with pentobarbital sodium. The effects of acute respiratory and metabolic acidosis and alkalosis were then examined. Decreases in systemic pH during respiratory acidosis caused equivalent increases in net water (54 +/- 8 microliters . cm-1 . h-1) and Na absorption (7 +/- 1 mu eq . cm- . h-1) and smaller increases in Cl absorption in cholera toxin compared with saline loops. These increases reversed the net secretion of these ions observed during alkalemia in the cholera toxin loops to net absorption. Metabolic acidosis and alkalosis and respiratory compensation of systemic pH of these metabolic disorders also altered cholera toxin-induced secretion in a direction consistent with the pH change. The increase in net HCO3 secretion caused by cholera toxin was unaffected by the respiratory disorders and did not vary with the HCO3 concentration in the metabolic disorders. These findings suggest that the systemic acid-base disorders that characterize intestinal secretory states may themselves alter intestinal absorptive function and fluid losses.


2002 ◽  
Vol 282 (2) ◽  
pp. F341-F351 ◽  
Author(s):  
Tae-Hwan Kwon ◽  
Christiaan Fulton ◽  
Weidong Wang ◽  
Ira Kurtz ◽  
Jørgen Frøkiær ◽  
...  

Several members of the Na-HCO[Formula: see text] cotransporter (NBC) family have recently been identified functionally and partly characterized, including rkNBC1, NBCn1, and NBC3. Regulation of these NBCs may play a role in the maintenance of intracellular pH and in the regulation of renal acid-base balance. However, it is unknown whether the expressions of these NBCs are regulated in response to changes in acid-base status. We therefore tested whether chronic metabolic acidosis (CMA) affects the abundance of these NBCs in kidneys using two conventional protocols. In protocol 1, rats were treated with NH4Cl in their drinking water (12 ± 1 mmol · rat−1 · day−1) for 2 wk with free access to water ( n = 8). Semiquantitative immunoblotting demonstrated that whole kidney abundance of NBCn1 and NBC3 in rats with CMA was dramatically increased to 995 ± 87 and 224 ± 35%, respectively, of control levels ( P < 0.05), whereas whole kidney rkNBC1 was unchanged (88 ± 14%). In protocol 2, rats were given NH4Cl in their food (10 ± 1 mmol · rat−1 · day−1) for 7 days, with a fixed daily water intake ( n = 6). Consistent with protocol 1, whole kidney abundances of NBCn1 (262 ± 42%) and NBC3 (160 ± 31%) were significantly increased compared with controls ( n = 6), whereas whole kidney rkNBC1 was unchanged (84 ± 17%). In both protocols, immunocytochemistry confirmed upregulation of NBCn1 and NBC3 with no change in the segmental distribution along the nephron. Consistent with the increase in NBCn1, measurements of pH transients in medullary thick ascending limb (mTAL) cells in kidney slices revealed two- to threefold increases in DIDS- sensitive, Na+-dependent HCO[Formula: see text] uptake in rats with CMA. In conclusion, CMA is associated with a marked increase in the abundance of NBCn1 in the mTAL and NBC3 in intercalated cells, whereas the abundance of NBC1 in the proximal tubule was not altered. The increased abundance of NBCn1 may play a role in the reabsorption of NH[Formula: see text] in the mTAL and increased NBC3 in reabsorbing HCO[Formula: see text].


2010 ◽  
Vol 30 (5) ◽  
pp. 63-69 ◽  
Author(s):  
Melissa Beaudet Jones

What are the basic concepts of acid-base balance, the 2 types of metabolic acidosis, and the common causes of each type of metabolic acidosis?


2018 ◽  
Vol 1 (1) ◽  
pp. 21-25
Author(s):  
Raymond Azar ◽  
Vincent Coevoet

Acid-base status of patients on peritoneal dialysis is influenced by multiple factors. Metabolic acidosis is a common feature of chronic renal failure and dialysis treatment provides alkali in the dialysate in order to maintain a normal acid-base balance. This paper reports the prevalence of acid-base disorders in peritoneal dialysis patients and their associations with clinical and laboratory parameters. This is a cross-sectional retrospective study that included all PD patients registered in the RDPLF database. Metabolic acidosis was found in 20.4% of patients while 27.8% of patients had metabolic alkalosis. There is a significant relationship between age, protein intake estimated by nPNA and the level of alkaline reserve pleading in favor of the influence of dietary intakes in the maintenance of metabolic acidosis. Low residual renal function is associated with a lower probability of being in metabolic alkalosis. These results could allow an individual choice of the dialysate buffer in order to permanently obtain stable acid-base status in patients on peritoneal dialysis.


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