Effect of Citrate Infusion on Urinary Aluminium Excretion in the Rat

1994 ◽  
Vol 86 (2) ◽  
pp. 223-226 ◽  
Author(s):  
Malcolm Cochran ◽  
Vira Chawtur ◽  
John W. Phillips ◽  
Beverley Dilena
Keyword(s):  
Glomerular Filtration Rate ◽  
Plasma Level ◽  
Glomerular Filtration ◽  
Filtration Rate ◽  
Excretion Rate ◽  
Urine Flow ◽  
Distilled Water ◽  
Aluminium Level ◽  
Excretion Rates ◽  
Urinary Citrate

1. Seven pairs of rats received 1 mmol/l aluminium citrate in their drinking water 5 days before the experiments. Five additional rats were treated identically. Six rats received the same food but drank distilled water. 2. After a 6 h fast, the animal was anaesthetized, the jugular vein and femoral artery were cannulated and the bladder was catheterized, after which an intravenous infusion of Hartmann's solution containing [14C]inulin was begun. The urine was collected at 20 min intervals and 1 ml of arterial blood was obtained before the end of each collection. After at least two basal collections, the infusion was modified to contain, in addition, 5 mmol/l NaHCO3 (control) or 5 mmol/l sodium citrate (experimental). The infusion rate, constant in each pair, differed between pairs across the range 60–125 μmol/min. 3. A total of eight collections was made per animal and urine flow, glomerular filtration rate, plasma and urinary aluminium and citrate were measured. 4. Control and experimental rats had a higher mean basal plasma aluminium level (0.39 ± 0.21 μmol/l) than the six rats receiving distilled water (0.16 ± 0.14 mmol/l, P < 0.001). The corresponding urinary aluminium excretion rates were similar (46 ± 31 and 47 ± 23 pmol/min, respectively). There was no significant difference between the basal values of any variable in the control and experimental rats. No significant change was observed in any variable during the infusion of NaHCO3 (controls). Among the experimental rats, there was no significant change in urine flow, glomerular filtration rate or plasma aluminium level. However, the plasma citrate level rose rapidly with the infusion to approach a plateau value in each case, and there were slower rises in urinary citrate and aluminium excretion rates. A renal threshold for citrate appeared to occur at a plasma level of approximately 0.25 mmol/l. The aluminium excretion rate was directly related to the citrate excretion rate (P < 0.01) and the increase in urinary aluminium excretion rate above the basal state was even more closely related (P < 0.001). 5. In the five additional animals pretreated with aluminium, the median ultrafiltrable aluminium was 20% (range 17–24%) of the total plasma level and no change was produced by citrate infused at the maximal rate. The plasma protein concentration also remained unchanged despite the fluid load. 6. We conclude that increased urinary citrate excretion is directly associated with an increase in aluminium excretion in aluminium-loaded animals. The data suggest that this increased excretion is independent of filtered load of aluminium and may therefore be the result of changes in handling of the metal within the kidney.

Lack of Dependence of Urine Pco2 upon Reduction of Glomerular Filtration Rate in Alkalotic Dogs

1977 ◽  
Vol 52 (2) ◽  
pp. 119-123
Author(s):  
B. J. Stinebaugh ◽  
T. H. Hostetter ◽  
R. A. Peraino ◽  
F. X. Schloeder ◽  
W. N. Suki
Keyword(s):  
Glomerular Filtration Rate ◽  
Glomerular Filtration ◽  
Filtration Rate ◽  
Urine Flow ◽  
Hydrogen Ion ◽  
Alkaline Urine ◽  
Ion Secretion ◽  
Arterial Blood ◽  
Excretion Rates ◽  
Acute Changes

1. The Pco2 gradient between alkaline urine and arterial blood (U—B Pco2) is thought to depend primarily on distal hydrogen ion secretion. However, other variables affecting the U—B Pco2 include the urine flow rate, the urinary bicarbonate and phosphate excretion rates and the glomerular filtration rate. 2. In order to evaluate the effects of acute changes in these factors on the U—B Pco2, bicarbonate-loaded dogs with maximal U—B Pco2 values were subjected to either acute unilateral elevations of ureteral pressure or hypotension caused by nitroprusside infusion. The results demonstrate that acute reduction in the glomerular fiitration rate does not cause a decrease in the U—B Pco2 as long as the urinary concentrations of phosphate and bicarbonate do not decline. 3. Urinary concentrations of phosphate and bicarbonate appeared more important than their excretion rates in the maintenance of elevated U—B Pco2 values.

The Role of Prostaglandins in Glucagon-Induced Natriuresis

1980 ◽  
Vol 58 (5) ◽  
pp. 393-401 ◽  
Author(s):  
M. A. Kirschenbaum ◽  
E. T. Zawada
Keyword(s):  
Glomerular Filtration Rate ◽  
Glomerular Filtration ◽  
Flow Rate ◽  
Sodium Excretion ◽  
Filtration Rate ◽  
Prostaglandin Synthesis ◽  
Urine Flow ◽  
Prostaglandin E ◽  
Excretion Rates

1. Three groups of anaesthetized dogs were studied to determine the role of renal prostaglandins in glucagon-induced natriuresis. 2. Urine flow, sodium and prostaglandin E excretion rates increased significantly in the experimental kidney with glucagon infusion (0.20 μg/min) into the renal artery. These changes were completely reversed after the administration of either of two inhibitors of prostaglandin synthesis. 3. Infusion of glucagon (0.20 μg/min) after the administration of either of the prostaglandin synthetase inhibitors failed to increase either urine flow rate or sodium excretion above control values and failed to elevate urine prostaglandin E excretion rates. 4. Infusion of glucagon (0.75–1.25 μg/min) resulted in significant elevations in urine flow rate, glomerular filtration rate, renal plasma flow, urine sodium and prostaglandin E excretion rates. 5. The data presented indicate that the diuresis and natriuresis seen with the infusion of glucagon (0.20 μg/min) are accompanied by an increase in urine prostaglandin E excretion and are reversed by the administration of inhibitors of prostaglandin synthesis, suggesting that the increased urine flow and sodium excretion rates are dependent on prostaglandin-mediated mechanisms. The administration of glucagon in higher doses appears to be associated with alterations in electrolyte excretion and glomerular filtration rate, which presumably is related to factors other than prostaglandin synthesis and release.

Amiloride-sensitive lithium reabsorption during doxazosin-induced blood pressure reduction in rats

1991 ◽  
Vol 81 (6) ◽  
pp. 809-814 ◽  
Author(s):  
Jørgen Søberg Petersen ◽  
Michael Shalmi ◽  
Martin Bak ◽  
Niels Lomholt ◽  
Sten Christensen
Keyword(s):  
Blood Pressure ◽  
Glomerular Filtration Rate ◽  
Glomerular Filtration ◽  
Mean Arterial Blood Pressure ◽  
Sodium Excretion ◽  
Filtration Rate ◽  
Excretion Rate ◽  
Urine Flow ◽  
Lithium Clearance ◽  
Arterial Blood

1. The effects of acute systemic α1-anoceptor blockade by doxazosin on glomerular filtration rate, urine flow, sodium clearance and lithium clearance were investigated in acutely prepared conscious rats. 2. Clearance experiments were performed during water diuresis (20 mmol/l NaCl and 110 mmol/l glucose, 3 ml/h). After a control period, animals were randomized to one of the following treatments: time-control (n = 9), doxazosin (50 μg primer; 30 μg h−1 kg−1) (n = 10), amiloride (1 mg primer; 2.4 mg h−1 kg−1) (n = 10) and doxazosin plus amiloride (n = 9). 3. Doxazosin reduced the mean arterial blood pressure from 125 to 108 mmHg; this was associated with transient reductions in glomerular filtration rate, urine flow and lithium clearance. After the transient anti-diuresis, the sodium excretion rate remained reduced in doxazosin-infused animals. Amiloride increased the sodium excretion rate without having effects on other variables. When doxazosin was given together with amiloride, the reduction in lithium clearance observed during the transient reduction in glomerular filtration rate and urine flow, was partly abolished. Thus the fractional lithium excretion was transiently increased in rats given doxazosin plus amiloride (from 29 to 40%), whereas in rats given doxazosin alone a non-significant reduction was observed (from 28 to 25%). The dissociation between lithium clearance and fractional lithium excretion in the two doxazosin-infused groups was only significant during the transient reduction in glomerular filtration rate and urine flow. 4. The results provide evidence for an amiloride-sensitive lithium reabsorption during acute systemic α1-adrenoceptor blockade. It is suggested that activation of baroreflexes during the acute reduction in mean arterial blood pressure is responsible for stimulation of distal lithium reabsorption by an unknown mechanism.

Effects of blood pH changes on potassium excretion in the dog

1962 ◽  
Vol 202 (4) ◽  
pp. 768-772 ◽  
Author(s):  
Charles Toussaint ◽  
Pierre Vereerstraeten
Keyword(s):  
Glomerular Filtration Rate ◽  
Proximal Tubule ◽  
Glomerular Filtration ◽  
Filtration Rate ◽  
Excretion Rate ◽  
Distal Tubule ◽  
Potassium Excretion ◽  
Ph Changes ◽  
Blood Ph ◽  
Ph Level

K+ excretion rate was measured at normal as well as at rising plasma K+ concentration in intact, in K-depleted, and in acetazolamide-treated dogs submitted to acute blood pH changes. The results indicate that, for any given value of glomerular filtration rate, K+ excretion rate is determined by at least three factors: 1) plasma K+ concentration, 2) blood pH level, and 3) presumably, the H+ gradient across the luminal border of the distal tubule. The data further suggest that most of the filtered K+ is reabsorbed by the proximal tubule, even in conditions of high filtered loads.

DIAGNOSIS AND TREATMENT: ACUTE RENAL FAILURE

PEDIATRICS ◽  
1965 ◽  
Vol 35 (3) ◽  
pp. 478-481
Author(s):  
Malcolm A. Holliday
Keyword(s):  
Renal Failure ◽  
Acute Renal Failure ◽  
Glomerular Filtration Rate ◽  
Renal Disease ◽  
Glomerular Filtration ◽  
Filtration Rate ◽  
Obstructive Uropathy ◽  
Urine Flow ◽  
Water Restriction ◽  
Plasma Electrolyte

ACUTE RENAL FAILURE is an uncommon emergency which faces pediatricians. It is usually easy to recognize. The management in the early phase is critical to the survival potential of the patient. The purpose of this review is to cite the causes, characteristics, and principally the management of acute renal failure. Renal failure is defined as a state in which there is not sufficient kidney function to prevent the development of severe uremia or to maintain plasma electrolyte values in a range compatible with ordinary activities. Clinically the condition is associated with mental confusion, stupor, and frequently convulsions. Persistent hiccoughs, irregular respirations, and muscle cramps also may occur. Usually though not always, there is obvious oliguria. Since urine flow is ordinarily but 0.2-2,0% of glomerular filtration rate, and since glomerular filtration rate reduction to 5-10% may be associated with uremia, it is possible to have renal failure without oliguria. It is also possible to have physiological oliguria (&lt; 300 ml per square meter) in response to rigid water restriction that is not related to renal failure. Hence, the term must be defined in terms of its effect on plasma composition rather than in terms of urine flow. The presence of certain clinical conditions known to result in acute renal failure should alert the physician. These include: nephrotoxie agents; hemoglobinuria or myoglobinuria; shock with anoxic damage; acute, diffuse renal disease; acute dehydration in patients with chronic advanced renal disease; and acute obstructive uropathy. Nephrotoxic agents, hemoglobinuria, and shock all result in acute tubular necrosis, and recovery depends upon the capacity of the nephron to regenerate on an intact basement membrane.

P0035URINARY CITRATE AS A MARKER OF RENAL FUNCTION IN PATIENTS WITH AUTOSOMAL DOMINANT POLYCYSTIC KIDNEY DISEASE

2020 ◽  
Vol 35 (Supplement_3) ◽  
Author(s):  
Francisco-Jose Borrego-Utiel ◽  
Isidoro Herrera ◽  
Enoc Merino Garcia ◽  
Clara Moriana Dominguez ◽  
Victoria Camacho Reina ◽  
...  
Keyword(s):  
Uric Acid ◽  
Glomerular Filtration Rate ◽  
Kidney Disease ◽  
Glomerular Filtration ◽  
Filtration Rate ◽  
Autosomal Dominant ◽  
Urinary Calcium ◽  
Polycystic Kidney ◽  
Autosomal Dominant Polycystic Kidney ◽  
Urinary Citrate

Abstract Background and Aims In autosomal dominant polycystic kidney disease (ADPKD) is frequent to find low urinary citrate levels. Recently it has been suggested that urinary citrate could be a marker of covert metabolic acidosis. Our aim was to analyze relationship between urinary citrate levels and renal functionality in ADPKD patients. Method We determined citrate, calcium and uric acid in 24-hour collected urine from 91 ADPKD patients Results Urinary citrate/creatinine ratio was 214±158 (range 5.3-678) mg/g Cr with levels significantly higher in females. When considering chronic kidney disease (CKD) stages we observed a progressive decrease in urinary osmolality and in urinary citrate, calcium and uric acid elimination. Low levels of citrate (&lt;300 mg/g Cr) were present in 40% in CKD-1 stage, in 69.7% in CKD-2 stage, 92% in CKD-3 stage and 100% in CKD-4 + 5 stages. Urinary citrate was correlated with serum creatinine (r= -0.66, p&lt;0.001) and eGFR (r= 0.56, p&lt;0.001). Urinary citrate significantly correlated with urinary calcium but correlation with urinary uric acid was weaker. We did not find any correlation with serum bicarbonate. Using multiple lineal regression analysis we found as predictors of urinary citrate to glomerular filtration rate, female gender and urinary calcium levels. In a subgroup of patients we measured total kidney volume and we found an inverse correlation with urinary citrate levels that dissappeared when it was corrected with glomerular filtration rate. We did not also find a relationship between urinary elimination of calcium or uric acid and TKV after adjusting with eGFR. Conclusion Urinary citrate is very frequently reduced in ADPKD patients being present from very early CKD stages. Their levels are inversely correlated with glomerular filtration rate and directly with urinary calcium excretion. We did not found a relathionship with serum bicarbonate. We think that it would be interesting to study urinary citrate in other nephropathies and verify if it could be a marker of covert metabolic acidosis.

Meclofenamate and urine concentration with and without exposure of the renal papilla

1981 ◽  
Vol 240 (5) ◽  
pp. F423-F429 ◽  
Author(s):  
R. J. Roman ◽  
C. Lechene
Keyword(s):  
Glomerular Filtration Rate ◽  
Glomerular Filtration ◽  
Filtration Rate ◽  
Urine Osmolality ◽  
Urine Concentration ◽  
Prostaglandin Synthesis ◽  
Urine Flow ◽  
Renal Papilla ◽  
Arterial Blood ◽  
Pelvic Urine

The recent finding that inhibitors of prostaglandin synthesis prevent the fall in urine concentration produced by papillary exposure challenges the hypothesis that contact between the pelvic urine and papilla is essential to the renal concentrating process. The present study examines the change in urine osmolality produced by exposure of the renal papilla in rats given meclofenamate. In control animals urine osmolality(Uosmol) decreased 57% after 2 h of exposure of the renal papilla. In rats given meclofenamate 4 mg/kg urine osmolality increased 16%, urine flow decreased 30%, and glomerular filtration rate was unchanged in the nonexposed kidney. Meclofenamate, however, did not alter the decrease in Uosmol seen in the kidney with the exposed papilla. Meclofenamate 10 mg/kg was also ineffective in preventing the fall in urine osmolality produced by papillary exposure, although this higher dose decreased glomerular filtration rate and arterial blood pressure. These results are consistent with the finding that pelvic urine urea is important to the urinary concentrating process and with the hypothesis that urine osmolality falls after papillary exposure because contact between pelvic urine and papilla is interrupted.

Supersensitivity to norepinephrine in chronically denervated kidneys: evidence for a postsynaptic effect

1987 ◽  
Vol 65 (11) ◽  
pp. 2219-2224 ◽  
Author(s):  
J. Krayacich ◽  
R. L. Kline ◽  
P. F. Mercer
Keyword(s):  
Blood Flow ◽  
Glomerular Filtration Rate ◽  
Glomerular Filtration ◽  
Renal Blood Flow ◽  
Sodium Excretion ◽  
Filtration Rate ◽  
Fractional Excretion ◽  
Urine Flow ◽  
Fractional Excretion Of Sodium ◽  
Infusion Of Norepinephrine

Denervation supersensitivity in chronically denervated kidneys increases renal responsiveness to increased plasma levels of norepinephrine. To determine whether this effect is caused by presynaptic (i.e., loss of uptake) or postsynaptic changes, we studied the effect of continuous infusion of norepinephrine (330 ng/min, i.v.) and methoxamine (4 μg/min, i.v.), an α1 adrenergic agonist that is not taken up by nerve terminals, on renal function of innervated and denervated kidneys. Ganglionic blockade was used to eliminate reflex adjustments in the innervated kidney and mean arterial pressure was maintained at preganglionic blockade levels by an infusion of arginine vasopressin. With renal perfusion pressure controlled there was a significantly greater decrease in renal blood flow (−67 ± 9 vs. −33 ± 8%), glomerular filtration rate (−60 ± 9 vs. −7 ± 20%), urine flow (−61 ± 7 vs. −24 ± 11%), sodium excretion (−51 ± 15 vs. −32 ± 21%), and fractional excretion of sodium (−50 ± 9 vs. −25 ± 15%) from the denervated kidneys compared with the innervated kidneys during the infusion of norepinephrine. During the infusion of methoxamine there was a significantly greater decrease from the denervated compared with the innervated kidneys in renal blood flow (−54 ± 10 vs. −30 ± 14%), glomerular filtration rate (−51 ± 11 vs. −19 ± 17%), urine flow (−55 ± 10 vs. −39 ± 10%), sodium excretion (−70 ± 9 vs. −59 ± 11%), and fractional excretion of sodium (−53 ± 10 vs. −41 ± 10%). These results suggest that vascular and tubular supersensitivity to norepinephrine in chronically denervated kidneys is due to postsynaptic changes involving α1-adrenergic receptors.

Excretion of progastrin products in human urine

1999 ◽  
Vol 276 (4) ◽  
pp. G985-G992 ◽  
Author(s):  
C. Palnaes Hansen ◽  
J. P. Goetze ◽  
F. Stadil ◽  
J. F. Rehfeld
Keyword(s):  
Glomerular Filtration Rate ◽  
Glomerular Filtration ◽  
Filtration Rate ◽  
Plasma Concentrations ◽  
Metabolic Clearance ◽  
Metabolic Clearance Rate ◽  
Renal Handling ◽  
Renal Metabolism ◽  
Tubular Transport ◽  
Excretion Rates

The renal handling of carboxyamidated gastrins, NH2-terminal progastrin fragments, and glycine-extended gastrins was examined in healthy volunteers. The respective urinary clearances after a meal amounted to 0.09 ± 0.02%, 0.17 ± 0.04% ( P< 0.05), and 0.04 ± 0.01% ( P< 0.01) of the glomerular filtration rate. During intravenous infusion of carboxyamidated gastrin-17, progastrin fragment-(1—35), and glycine-extended gastrin-17, the respective urinary clearances amounted to 0.08 ± 0.02, 0.46 ± 0.08, and 0.02 ± 0.01%, respectively, of the glomerular filtration rate. The metabolic clearance rate of the three peptides was 24.4 ± 1.3, 6.0 ± 0.4, and 8.6 ± 0.7 ml ⋅ kg−1⋅ min−1. A maximum rate for tubular transport or degradation of the peptides could not be determined, nor was a renal plasma threshold recorded. Plasma concentrations and urinary excretion rates correlated for gastrin-17 and progastrin fragment-(1—35) ( r = 0.94 and 0.97, P < 0.001), whereas the excretion of glycine-extended gastrin diminished with increasing plasma concentrations. We conclude that renal excretion of progastrin products is negligible compared with renal metabolism and that renal handling of the peptides depends on their molecular structure. Hence, the kidneys exhibited a higher excretion of NH2-terminal progastrin fragments than of carboxyamidated and especially glycine-extended gastrins.

scholarly journals MicroRNAs in the Progress of Diabetic Nephropathy: A Systematic Review and Meta-Analysis

2019 ◽  
Vol 2019 ◽  
pp. 1-9 ◽  
Author(s):  
Li-ping Wang ◽  
Yu-zhen Gao ◽  
Bin Song ◽  
Guo Yu ◽  
Hui Chen ◽  
...  
Keyword(s):  
Systematic Review ◽  
Diabetic Nephropathy ◽  
Glomerular Filtration Rate ◽  
Glomerular Filtration ◽  
Filtration Rate ◽  
Urinary Albumin Excretion ◽  
Meta Analysis ◽  
Group Versus ◽  
Urinary Albumin ◽  
Excretion Rates

Background. We conducted a systematic review and meta-analysis of existing literature to evaluate the different outcomes of microRNAs (miRNAs) in diabetic nephropathy (DN), including urinary albumin excretion rates, urinary albumin creatinine rates, glomerular filtration rate, HbAc1, and creatinine.Methods. Electronic databases including PUBMED, MEDLINE, and EMBASE were searched for eligible publications to July 2018. The following comparisons between treatment groups were included: normal group versus DN group; control group versus micro/macroalbuminuria group.Results. Twelve eligible studies that included 2500 participants were finally recruited in this meta-analysis. Fifteen miRNAs (miRNA-21, miRNA-181b, miRNA-194, miRNA-30, miRNA-215, and others) were upregulated whereas seven miRNAs (miRNA-26a, miRNA-126, miRNA-424, miRNA-574-3p, miR-223, miR-155, and miR-192) were downregulated in the DN group compared with control groups. The miR-133b, miR-342, miR-30, miR-192, miR-194, and miR-215 were significantly correlated in urinary albumin excretion rates (r=0.33, 95% CI= 0.26-0.39). miR-192, miR-217, miR-15b, miR-34a, and miR-636 were correlated with urinary albumin creatinine rates (r=0.69; 95% CI=0.12-0.92), while miR-133b, miR-345, miR-33, miR-326, miR-574-3p, miR-126, miR-217, miR-15b, miR-34a, and miR-636 were significantly correlated with HbAc1 (r =0.23, 95% CI = 0.15-0.31). There were twelve miRNAs that were closely related to the glomerular filtration rate (r=0.28, 95% CI =0.21-0.34). Creatinine (r=0.33, 95% CI = 0.22-0.40) was significantly different between normal and DN groups.Conclusions. The meta-analysis acquired the correlations between miRNAs and outcomes including UAER, UACR, eGFR, HbAc1, and creatinine in DN. It suggested that miRNAs may participate in the pathogenesis of DN process.

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