Tubular function

2015 ◽  
Author(s):  
Marijn Speeckaert ◽  
Joris Delanghe
Keyword(s):  
Fractional Excretion ◽  
Tubular Function ◽  
Tubular Dysfunction ◽  
Renal Fanconi Syndrome ◽  
Glomerular Function ◽  
Diminished Capacity ◽  
Fractional Excretion Of Sodium ◽  
Proximal Tubular ◽  
Pass Through ◽  
Renal Tubular

Assessment of tubular function is more complicated than the measurement of glomerular filtration rate. Different functions may be affecting according to the different segments of tubule involved. Key tests include concentrating and diluting capacity, and fractional excretion of sodium. Tubular proteinuria occurs when glomerular function is normal, but when the proximal tubules have a diminished capacity to reabsorb and to catabolize proteins, causing an increased urinary excretion of the low-molecular-mass proteins that normally pass through the glomerulus. Proximal tubular dysfunction is characterized by hypophosphataemia, and a variety of other abnormalities characteristics of the renal Fanconi syndrome. Distinguishing the location of the lesion in Renal Tubular Acidosis is considered in Chapter 35.

Polyuria and impaired renal blood flow after asphyxia in preterm fetal sheep

2004 ◽  
Vol 286 (3) ◽  
pp. R576-R583 ◽  
Author(s):  
J. S. Quaedackers ◽  
V. Roelfsema ◽  
C. J. Hunter ◽  
E. Heineman ◽  
A. J. Gunn ◽  
...  
Keyword(s):  
Blood Flow ◽  
Renal Blood Flow ◽  
Fractional Excretion ◽  
Analysis Of Covariance ◽  
Tubular Dysfunction ◽  
Renal Tubular Dysfunction ◽  
Fetal Sheep ◽  
Arterial Blood ◽  
Fractional Excretion Of Sodium ◽  
Renal Tubular

Renal impairment is common in preterm infants, often after exposure to hypoxia/asphyxia or other circulatory disturbances. We examined the hypothesis that this association is mediated by reduced renal blood flow (RBF), using a model of asphyxia induced by complete umbilical cord occlusion for 25 min ( n = 13) or sham occlusion ( n = 6) in chronically instrumented preterm fetal sheep (104 days, term is 147 days). During asphyxia there was a significant fall in RBF and urine output (UO). After asphyxia, RBF transiently recovered, followed within 30 min by a secondary period of hypoperfusion ( P < 0.05). This was mediated by increased renal vascular resistance (RVR, P < 0.05); arterial blood pressure was mildly increased in the first 24 h ( P < 0.05). RBF relatively normalized between 3 and 24 h, but hypoperfusion developed again from 24 to 60 h ( P < 0.05, analysis of covariance). UO significantly increased to a peak of 249% of baseline between 3 and 12 h ( P < 0.05), with increased fractional excretion of sodium, peak 10.5 ± 1.4 vs. 2.6 ± 0.6% ( P < 0.001). Creatinine clearance returned to normal after 2 h; there was a transient reduction at 48 h to 0.32 ± 0.02 ml·min-1·g-1(vs. 0.45 ± 0.04, P < 0.05) corresponding with the time of maximal depression of RBF. No renal injury was seen on histological examination at 72 h. In conclusion, severe asphyxia in the preterm fetus was associated with evolving renal tubular dysfunction, as shown by transient polyuria and natriuresis. Despite a prolonged increase in RVR, there was only a modest effect on glomerular function.

Glomerular and tubular function during AT1 receptor blockade in pigs with neonatal induced partial ureteropelvic obstruction

2007 ◽  
Vol 292 (3) ◽  
pp. F921-F929 ◽  
Author(s):  
Anni Eskild-Jensen ◽  
Klaus Thomsen ◽  
Christine Rungø ◽  
Luis S. Ferreira ◽  
Lene Fogt Paulsen ◽  
...  
Keyword(s):  
Collecting Duct ◽  
Fractional Excretion ◽  
At1 Receptor ◽  
Receptor Blockade ◽  
Glomerular Function ◽  
Contralateral Kidney ◽  
Diagnostic Potential ◽  
Fractional Excretion Of Sodium ◽  
Renal Sodium Handling ◽  
Immunohistochemical Analyses

Previously, we showed that neonatal induced chronic partial unilateral ureteral obstruction (PUUO) of the multipapillary pig kidney decreased glomerular filtration rate (GFR) of the obstructed kidney. We hypothesized that ANG II and nitric oxide (NO) are important for the changes in renal function and in the present study we examined the effects of chronic AT1 receptor blockade using CV-11974 (0.12 mg/h candesartan from age 23 to 30 days) on kidney function development after PUUO was induced in 2-day-old piglets. Moreover, the effect of superimposed acute NO inhibition using NG-nitro-l-arginine methyl ester (l-NAME; 15 mg/kg) was examined to identify if this has diagnostic potential. PUUO significantly increased GFR in the nonobstructed contralateral kidney independent of candesartan. In candesartan-treated piglets, the l-NAME-induced GFR reduction seen in normal and nonobstructed kidneys was absent in the partial obstructed kidneys. Urine output and fractional excretion of water were increased from the partial obstructed kidneys. Consistent with this immunohistochemical analyses showed a reduced aquaporin-2 labeling in the collecting duct principal cells. Moreover, renal sodium handling was compromised by PUUO evidenced by an increased fractional excretion of sodium which was enhanced by candesartan treatment. In conclusion, our findings suggest that the counterbalance between AT1 receptor-mediated vasoconstriction and NO-mediated vasodilatation which maintain GFR in normal young porcine kidneys is changed by neonatal induced chronic PUUO. This may have diagnostic potential in children with suspected congenital obstruction. Our results also demonstrate compromised tubular functions in response to chronic PUUO despite preservation of glomerular function.

Approach to the patient with renal Fanconi syndrome, glycosuria, or aminoaciduria

2018 ◽  
Author(s):  
Detlef Bockenhauer ◽  
Robert Kleta
Keyword(s):  
Fanconi Syndrome ◽  
Tubular Dysfunction ◽  
Renal Fanconi Syndrome ◽  
Renal Glycosuria ◽  
Proximal Tubular Dysfunction ◽  
Wide Range ◽  
Proximal Tubular ◽  
Proximal Tubular Function ◽  
Low Molecular Weight Proteins ◽  
Filtration Capacity

Up to 80% of filtered salt and water is returned back into the circulation in the proximal tubule. Several solutes, such as phosphate, glucose, low-molecular weight proteins, and amino acids are exclusively reabsorbed in this segment, so their appearance in urine is a sign of proximal tubular dysfunction. An entire orchestra of specialized apical and basolateral transporters, as well as paracellular molecules, mediate this reabsorption. Defects in proximal tubular function can be isolated (e.g. isolated renal glycosuria, aminoacidurias, or hypophosphataemic rickets) or generalized. In the latter case it is called the Fanconi–Debre–de Toni syndrome, based on the initial clinical descriptions. However, in clinical practice it is usually referred to as just the ‘renal Fanconi syndrome’. Severity of proximal tubular dysfunction can vary, and may coexist with some degree of loss of glomerular filtration capacity. Causes include a wide range of insults to proximal tubular cells, including a number of genetic conditions, drugs and poisons.

Unilateral nephrectomy and cisplatin as risk factors of ifosfamide-induced nephrotoxicity: analysis of 120 patients.

1994 ◽  
Vol 12 (1) ◽  
pp. 159-165 ◽  
Author(s):  
R Rossi ◽  
A Gödde ◽  
A Kleinebrand ◽  
M Riepenhausen ◽  
J Boos ◽  
...  
Keyword(s):  
Risk Factors ◽  
Renal Function ◽  
Unilateral Nephrectomy ◽  
Tubular Dysfunction ◽  
Schwartz Formula ◽  
Cytostatic Treatment ◽  
Fanconi’S Syndrome ◽  
Fractional Excretion Of Sodium ◽  
Proximal Tubular ◽  
Fanconi's Syndrome

PURPOSE This study was performed to identify risk factors of ifosfamide-induced renal damage. PATIENTS AND METHODS Renal function was assessed in 120 patients at a minimum of 3 months after completion of chemotherapy including ifosfamide. The cumulative ifosfamide dose ranged from 2 to 95 g/m2 (median, 30 g/m2). Ten patients had undergone unilateral nephrectomy; combination cytostatic treatment included cisplatin in 51 and methotrexate in 57. Sixty-eight patients had received gentamicin treatment. The glomerular filtration rate was estimated using the Schwartz formula. Proximal tubular function was assessed by the percent reabsorptions of glucose and 16 amino acids, the fractional excretion of sodium, and the fractional reabsorption of phosphate. In addition, the serum bicarbonate level was measured. RESULTS Proximal tubular dysfunction--with a predominance of renal amino acid (66.3%) and phosphate loss (38.3%)--was much more frequent than both glomerular impairment and acidosis. Seven patients were identified as having renal Fanconi's syndrome, and generalized tubulopathy was noted in another 15 patients. Ifosfamide-induced nephrotoxicity was dose-dependent, with a weak linear inverse correlation between cumulative ifosfamide dose and fractional phosphate reabsorption. Unilateral nephrectomy proved to be the single most important risk factor (odds ratio for the development of renal Fanconi's syndrome, 11.4), but cisplatin also significantly enhanced ifosfamide-mediated nephrotoxicity. Methotrexate, gentamicin, and patient age at primary diagnosis had no influence on renal function. CONCLUSION Ifosfamide chemotherapy should probably be restricted in patients after unilateral nephrectomy.

Effect of vasoactive intestinal peptide on isolated perfused rat kidney

1985 ◽  
Vol 249 (5) ◽  
pp. E494-E497 ◽  
Author(s):  
R. M. Rosa ◽  
P. Silva ◽  
J. S. Stoff ◽  
F. H. Epstein
Keyword(s):  
Vasoactive Intestinal Peptide ◽  
Rat Kidney ◽  
Urine Volume ◽  
Fractional Excretion ◽  
Rectal Gland ◽  
Renal Nerves ◽  
Isolated Perfused Rat Kidney ◽  
Fractional Excretion Of Sodium ◽  
Perfused Rat Kidney ◽  
Renal Tubular

Vasoactive intestinal peptide, a polypeptide neurotransmitter, stimulates salt secretion by the mammalian intestine and the rectal gland of the dogfish shark. Because of the recent identification of vasoactive intestinal peptide in renal nerves, the present study was undertaken to investigate its effects on the isolated perfused rat kidney. The addition of vasoactive intestinal peptide to the recirculating perfusate produced a significant increase in urine volume, fractional excretion of sodium, chloride, and potassium, as well as osmolar clearance when compared with control kidneys. These changes associated with addition of vasoactive intestinal peptide occurred without any significant changes in perfusion flow, renal vascular resistance, or inulin clearance. These experiments strongly suggest an action of vasoactive intestinal peptide on renal tubular reabsorption.

Effect of Phlorhizin on Renal Glucose and Phosphate Transport in the Dog

1979 ◽  
Vol 57 (4) ◽  
pp. 367-374 ◽  
Author(s):  
Sung-Feng Wen
Keyword(s):  
Proximal Tubule ◽  
Sodium Transport ◽  
Fractional Excretion ◽  
Phosphate Transport ◽  
Reciprocal Relationship ◽  
Sodium Reabsorption ◽  
Group I ◽  
Glucose Reabsorption ◽  
Fractional Excretion Of Sodium ◽  
Proximal Tubular

1. Clearance and micropuncture studies were performed in 19 thyroparathyroidectomized dogs to examine the inter-relationship between the renal transport of sodium, glucose and phosphate. 2. All experiments were carried out before and after the intravenous administration of phlorhizin [7 mg (15 μmol)/kg] with a sustaining infusion of the same dose/h. Thirteen dogs were studied during hydropenia (group I) and six dogs in the volume-expanded state (group II). 3. In the proximal tubule, phlorhizin significantly reduced sodium reabsorption in hydropenic dogs, but had no effect in volume-expanded dogs. Proximal tubular glucose reabsorption was completely inhibited by phlorhizin in both groups, but no significant change in phosphate reabsorption was observed. 4. Fractional glucose excretion in the urine reached 83–89% after phlorhizin, values significantly less than 100%, suggesting a residual reabsorption of glucose in a more distal segment or in deep nephrons. The changes in fractional excretion of sodium and phosphate were significantly correlated. 5. The effect of phlorhizin on both sodium and glucose reabsorption in the proximal tubule in hydropenic dogs suggests the existence of a co-transport mechanism, whereas the absence of an effect on sodium transport in volume-expanded dogs despite complete inhibition of glucose reabsorption indicates the existence of a sodium-independent component of net proximal tubular glucose transport. 6. Absence of the effect of phlorhizin on proximal tubular phosphate transport in the face of a significant reduction in sodium reabsorption implies that the reciprocal relationship between glucose and phosphate transport could be masked by the changes in sodium transport. Thus the sodium-phosphate transport relationship may prevail over that of glucose-phosphate in the proximal tubule.

scholarly journals Assessment of Urinary Kidney Injury Molecule-1 as an Indicator of Early Renal Insult in Children with Cystic Fibrosis

2020 ◽  
Vol 8 (B) ◽  
pp. 262-267
Author(s):  
Walaa Shahin ◽  
Ahmed Bader ◽  
Rawdah Ahmed ◽  
Mona Alattar ◽  
Mona Alfalaki ◽  
...  
Keyword(s):  
Cystic Fibrosis ◽  
Urine Analysis ◽  
Kidney Injury ◽  
Fractional Excretion ◽  
Control Group ◽  
Renal Ultrasound ◽  
Fractional Excretion Of Sodium ◽  
Beta 2 ◽  
Renal Tubular ◽  
Kidney Injury Molecule 1

BACKGROUND: The risk of acute kidney injury in cystic fibrosis (CF) patients is due to renal tubular affection by CFTR gene. AIM: Our study aimed at early detection of renal impairment in CF patients, to enable careful monitoring and adjustment of nephrotoxic medications. METHODS: Fifty patients with CF were enrolled in our study; they were age- and sex-matched to 40 healthy control children. All subjects were screened by urine analysis, measurements of kidney function tests, fractional excretion of sodium, β2-microglobulin (beta-2-M) excretion, and renal ultrasound examination. Urinary kidney injury molecule-1 (KIM-1) was assayed using ELISA technique. RESULTS: Both urinary beta-2-M and KIM-1 concentrations were significantly higher in CF patients compared to the control group (p < 0.001). The duration of the disease was significantly positively correlated with the urinary beta-2-M and KIM-1 levels (r = 0.6 and 0.7, respectively; p < 0.01). CONCLUSIONS: Our results showed that urinary KIM-1 can be considered as a sensitive early indicator of acute renal injury.

Characterization of the Natriuresis Caused in Normal Man by Immersion in Water

1972 ◽  
Vol 43 (2) ◽  
pp. 275-287 ◽  
Author(s):  
M. Epstein ◽  
D. C. Duncan ◽  
L. M. Fishman
Keyword(s):  
Water Immersion ◽  
Control Period ◽  
Free Water ◽  
Fractional Excretion ◽  
Normal Male ◽  
Free Water Clearance ◽  
Fractional Excretion Of Sodium ◽  
Sodium Load ◽  
Proximal Tubular ◽  
Normal Man

1. The effects of 4–6 h of water immersion on the renal excretion of water and electrolytes were studied in thirteen normal male subjects in balance on a constant diet containing 150 mEq of Na and 100 mEq of K per day. Each subject was studied during a control period, consisting of quiet sitting, and during water immersion to the neck. 2. Immersion resulted in a natriuresis beginning within the first hour, with the rate of sodium excretion eventually exceeding that of the control period by 3–4-fold; potassium excretion also increased. Despite a progressively negative water balance during the immersion studies, urine flow was greater during the first 4 h and free water clearance was greater during the first 2 h of immersion than during the control study. 3. The demonstration of a highly significant increase in fractional excretion of sodium during immersion suggests that the natriuresis of water immersion is not attributable to changes in filtered sodium load. 4. The prompt onset of the natriuresis, the concomitant kaliuresis and the fact that aldosterone secretion under the conditions of study was probably already suppressed make it unlikely that the natriuresis of water immersion is mediated solely by decreases in aldosterone activity. 5. The data suggest that the natriuresis caused by water immersion is the result of decreased fractional reabsorption of sodium proximal to the renal diluting site. The mechanism whereby increased proximal tubular sodium rejection occurs in relation to immersion remains unclear.

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