scholarly journals Impaired Urine Dilution Capability in HIV Stable Patients

2014 ◽  
Vol 2014 ◽  
pp. 1-8 ◽  
Author(s):  
Waldo H. Belloso ◽  
Mariana de Paz Sierra ◽  
Matilde Navarro ◽  
Marisa L. Sanchez ◽  
Ariel G. Perelsztein ◽  
...  
Keyword(s):  
Hiv Infection ◽  
Proximal Tubule ◽  
Free Water ◽  
Antiretroviral Drugs ◽  
Control Group ◽  
Sodium Reabsorption ◽  
Thick Ascending Limb ◽  
Free Water Clearance ◽  
Proximal Tubular Function ◽  
Water Clearance

Renal disease is a well-recognized complication among patients with HIV infection. Viral infection itself and the use of some antiretroviral drugs contribute to this condition. The thick ascending limb of Henle’s loop (TALH) is the tubule segment where free water clearance is generated, determining along with glomerular filtration rate the kidney’s ability to dilute urine.Objective. We analyzed the function of the proximal tubule and TALH in patients with HIV infection receiving or not tenofovir-containing antiretroviral treatment in comparison with healthy seronegative controls, by applying a tubular physiological test, hyposaline infusion test (Chaimowitz’ test).Material & Methods. Chaimowitz’ test was performed on 20 HIV positive volunteers who had normal renal functional parameters. The control group included 10 healthy volunteers.Results. After the test, both HIV groups had a significant reduction of serum sodium and osmolarity compared with the control group. Free water clearance was lower and urine osmolarity was higher in both HIV+ groups. Proximal tubular function was normal in both studied groups.Conclusion. The present study documented that proximal tubule sodium reabsorption was preserved while free water clearance and maximal urine dilution capability were reduced in stable HIV patients treated or not with tenofovir.

Maleic acid-induced reabsorptive dysfunction in the proximal and distal nephron

1983 ◽  
Vol 245 (3) ◽  
pp. F339-F344
Author(s):  
E. D. Brewer ◽  
H. O. Senekjian ◽  
A. Ince ◽  
E. J. Weinman
Keyword(s):  
Proximal Tubule ◽  
Maleic Acid ◽  
Chloride Concentration ◽  
Free Water ◽  
Distal Nephron ◽  
Free Water Clearance ◽  
Total Inhibition ◽  
Clearance Studies ◽  
Distal Delivery ◽  
Water Clearance

Micropuncture and clearance studies were performed to assess reabsorptive function in the proximal and distal nephron of rats with experimental Fanconi's syndrome induced by maleic acid. Anesthetized rats were studied by free-flow micropuncture of the late proximal tubule 90-120 min after continuous intravenous administration of maleic acid, 100 mg X kg-1 X h-1. Compared with control rats, the reabsorption of sodium and phosphate was significantly reduced (P less than 0.001 and less than 0.02, respectively). Tubular fluid-to-ultrafiltrate (TF/UF) chloride concentration ratio was 1.00 +/- 0.02 compared with 1.16 +/- 0.03 (P less than 0.01) in controls, suggesting a nearly total inhibition of proximal bicarbonate reabsorption. Whole kidney fractional excretions of sodium and chloride were increased significantly (P less than 0.02) but could not be explained by enhanced delivery of these solutes out of the late proximal tubule. To assess whether distal nephron reabsorption of sodium and chloride were inhibited by maleic acid, clearance studies were performed during water diuresis in awake rats. During maleic acid administration, 200 mg X kg-1 X h-1, urine flow rate (P less than 0.02) and the fractional excretions of sodium and chloride (P less than 0.001) increased significantly, but fractional free water clearance decreased from 7.16 +/- 0.42 to 4.03 +/- 0.68% (P less than 0.001). In acetazolamide-treated control rats but not in maleic acid-treated rats with similar bicarbonaturia, the magnitude of fractional free water clearance closely approximated the simultaneously measured fractional distal delivery of chloride. These studies suggest that maleic acid inhibits reabsorption at a distal nephron site or sites as well as in the proximal tubule.

Aldosterone increases urine production and decreases apical AQP2 expression in rats with diabetes insipidus

2006 ◽  
Vol 290 (2) ◽  
pp. F438-F449 ◽  
Author(s):  
Jakob Nielsen ◽  
Tae-Hwan Kwon ◽  
Jeppe Praetorius ◽  
Jørgen Frøkiær ◽  
Mark A. Knepper ◽  
...  
Keyword(s):  
Creatinine Clearance ◽  
Diabetes Insipidus ◽  
Free Water ◽  
Sodium Balance ◽  
Apical Plasma Membrane ◽  
Sodium Reabsorption ◽  
Outer Medulla ◽  
Free Water Clearance ◽  
Urine Production ◽  
Water Clearance

Vasopressin and aldosterone are essential hormones in the regulation of water and sodium balance. Aldosterone regulates sodium reabsorption, although synergistic effects on collecting duct water permeability have been shown. We investigated the effects of 7-day aldosterone infusion or oral spironolactone treatment on water balance and aquaporin (AQP) 2 expression in rats with 21 days of lithium-induced nephrogenic diabetes insipidus (Li-NDI). In rats with Li-NDI, aldosterone markedly increased (271 ± 14 ml/24 h), whereas spironolactone decreased (74 ± 11 ml/24 h) urine production compared with rats treated with lithium only (120 ± 11 ml/24 h). Aldosterone increased free-water clearance and creatinine clearance, whereas spironolactone caused a decreased creatinine clearance but unchanged free-water clearance. Immunoblotting showed unchanged AQP2 expression in cortex/outer stripe of the outer medulla and inner medulla. In the inner stripe of the outer medulla aldosterone caused a decreased AQP2 expression, whereas spironolactone caused an increase compared with rats treated with lithium only. Semiquantitative confocal immunofluorescence microscopy of AQP2 immunolabeling showed reduced AQP2 expression in the apical plasma membrane domain in connecting tubule (CNT) and initial cortical collecting ducts (iCCD) in response to aldosterone-treated rats compared with rats treated with lithium only. Spironolactone significantly increased apical AQP2 expression in the iCCD compared with rats treated with lithium only. We also tested whether similar changes could be observed in vasopressin-deficient BB rats and found similar changes in urine production and subcellular AQP2 expression in the CNT and iCCD in response to aldosterone and spironolactone. This study shows that aldosterone treatment perturbs diabetes insipidus and is associated with AQP2 redistribution in CNT and iCCD likely mediated by the spironolactone-sensitive mineralocorticoid receptor.

Nonoxidative glucose metabolism a prerequisite for formation of dilute urine

1982 ◽  
Vol 242 (5) ◽  
pp. F491-F498
Author(s):  
A. D. Baines ◽  
B. D. Ross
Keyword(s):  
Glucose Metabolism ◽  
Free Water ◽  
Glucose Production ◽  
Inhibitory Effect ◽  
Sodium Reabsorption ◽  
Diluting Segment ◽  
Free Water Clearance ◽  
Water Excretion ◽  
Total Sodium ◽  
Water Clearance

To examine links between norepinephrine- (NE) stimulated sodium transport and gluconeogenesis, we perfused isolated rat kidneys with 6% albumin, containing various combinations of glucose, alanine, pyruvate. and lactate and inhibitors of gluconeogenesis (0.1 mM mercaptopicolinate, MP) or glucose metabolism (0.2-0.5 mM 2-deoxyglucose, DG). Inulin clearance, fractional potassium reabsorption, total sodium reabsorption, and free water clearance were higher in kidneys perfused with 5 mM glucose plus 2 mM alanine than in kidneys perfused with either 10 mM lactate or 5 mM pyruvate. NE, added after 40 min of perfusion, decreased fractional sodium and potassium excretion in all experiments. In lactate- and/or pyruvate-perfused kidneys NE decreased fractional water excretion with little increase in free water clearance; free water formation was lowest in kidneys perfused with DG or MP. Glucose (5 mM) reversed the inhibitory effect of MP on free water clearance. In glucose-perfused kidneys NE did not decrease fractional water excretion, whereas free water clearance increased threefold. NE stimulated glucose production from pyruvate 2.4-fold and from lactate 1.6-fold. MP inhibited gluconeogenesis both in the basal state and after NE. We conclude that the formation of dilute urine requires nonoxidative glucose metabolism to maintain low water permeability in the diluting segment and a high peritubular glucose concentration that is ensured by gluconeogenesis in adjacent proximal tubules.

Dysfunction of the proximal tubule underlies maleic acid-induced type II renal tubular acidosis

1982 ◽  
Vol 243 (6) ◽  
pp. F604-F611 ◽  
Author(s):  
H. A. Al-Bander ◽  
R. A. Weiss ◽  
M. H. Humphreys ◽  
R. C. Morris
Keyword(s):  
Proximal Tubule ◽  
Renal Tubular Acidosis ◽  
Maleic Acid ◽  
Free Water ◽  
Fractional Excretion ◽  
Thick Ascending Limb ◽  
Type Ii ◽  
Free Water Clearance ◽  
Plasma Bicarbonate ◽  
Renal Tubular

To investigate whether dysfunction of the proximal tubule underlies maleic acid-(MA) induced type II (“proximal”) renal tubular acidosis (RTA II), we intravenously administered either MA or acetazolamide to eight conscious trained dogs undergoing water diuresis and examined the relationship between fractional solute-free water clearance (Ch2o/GFR), a measure of NaCl reabsorption in the post-proximal nephron, and either fractional urine flow (V/GFR), a measure of total solute rejected by the proximal tubule, or the sum of fractional excretion of Cl- and Ch2o/GFR [(Ccl + Ch2o)/GFR], a measure of proximally rejected solute that is potentially reabsorbable by the thick ascending limb. When MA or acetazolamide induced brisk bicarbonaturia at normal plasma bicarbonate concentrations: 1) V/GFR, (Ccl + Ch20)GFR, and Ch2o/GFR increased strikingly; 2) at any increment of Ch2o/GFR ws not; 3) the increments of V/GFR correlated positively with those of fractional excretion of bicarbonate (P less than 0.001); 4) during hyperchloremic acidosis, MA-induced bicarbonaturia was greatly attenuated; the increment in V/GFR was halved and approximated that in Ch20/GFR, which was unchanged; 5) when plasma bicarbonate was abruptly increased, bicarbonaturia increased strikingly and V/GFR increased further but Ch20/GFR and aminoaciduria did not. We conclude that MA induces a reduction in the net rate at which the proximal tubule reabsorbs HCO-3, Na+, and Cl-. This dysfunction underlies RTA II and evokes greatly increased reabsorption of Cl- and Na+ in the post-proximal tubule.

Bicarbonate and sodium reabsorption by the isolated perfused kidney

1975 ◽  
Vol 228 (5) ◽  
pp. 1525-1530 ◽  
Author(s):  
A Besarab ◽  
P Silva ◽  
B Ross ◽  
FH Epstein
Keyword(s):  
Rat Kidney ◽  
Large Fraction ◽  
Free Water ◽  
Sodium Reabsorption ◽  
Renal Tubules ◽  
Free Water Clearance ◽  
Isolated Perfused Kidney ◽  
Bicarbonate Reabsorption ◽  
Perfused Kidney ◽  
Water Clearance

The role of bicarbonate reabsorption and of transtubular chloride gradients in the bulk reabsorption of sodium and water by renal tubules can be tested in the isolated perfused kidney by perfusing with a medium from which bicarbonate has been omitted. Perfusion of the isolated rat kidney with an artificial medium in which bicarbonate is replaced by chloride results in a fall in fractional reabsorption of sodium from 97 to 84%. Stepwise restoration of bicarbonate concentration in the perfusion medium to 25 meq/liter is associated with a parallel recovery of sodium reabsorption to control levels. Inhibition of bicarbonate reabsorption with acetazolamide produces a slightly smaller reduction in sodium reabsorption (97-89%), an effect not seen in the absence of bicarbonate. Acetazolamide greatly increases phosphate excretion and free water clearance in a way consistent with suppression of proximal tubular reabsorption. By contrast, simple omission of bicarbonate from the perfusing medium does not alter phosphaturia or free water clearance. Reabsorption of bicarbonate appears to account for a fraction of sodium reabsorption roughly equivalent to the proportion of sodium associated stoichiometrically with bicarbonate in the glomerule filtrate. The data do not support the hypothesis that the development of a transtubular chloride gradient is critically important for the reabsorption of a large fraction of the glomerular filtrate.

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