Exaggerated Fractional Sodium Excretion in Hypertension with Advanced Renal Disease: The Role of Renal Prostaglandin and Kallikrein

1981 ◽  
Vol 61 (s7) ◽  
pp. 327s-330s ◽  
Author(s):  
Keishi Abe ◽  
Yutaka Imai ◽  
Makito Sato ◽  
Toshiaki Haruyama ◽  
KO Sato ◽  
...  
Keyword(s):  
Renal Disease ◽  
Urinary Excretion ◽  
Creatinine Clearance ◽  
Sodium Excretion ◽  
Prostaglandin E ◽  
Borderline Hypertension ◽  
Fractional Sodium Excretion ◽  
Sustained Hypertension ◽  
Renal Tubular

1. The role of renal prostaglandin E (PGE) and kallikrein in the mechanism of the exaggerated fractional sodium excretion in hypertensive patients with advanced renal disease was investigated. 2. Urinary excretion of PGE and kallikrein was significantly decreased in patients with sustained hypertension. 3. Four times higher values for fractional sodium excretion and four or five times higher values for the urinary excretion of PGE corrected for creatinine clearance were found in patients with sustained hypertension. There was a significant positive correlation (r = 0.677) between the two, suggesting that PGE in the renal tubular compartment may be involved in the mechanism of the exaggerated fractional Na excretion in patients with advanced renal disease. 4. The urinary excretion rate of kallikrein corrected for creatinine clearance was three times greater in patients with borderline hypertension, but not significantly increased in those with sustained hypertension, compared with that in healthy volunteers.

Role of Fractional Sodium Excretion in patients with Refractory Hypertension

2021 ◽  
Vol 0 (0) ◽  
pp. 0-0
Author(s):  
Ahmed El-Tahawy ◽  
Mohammad Mohammad ◽  
Magdy AbdSamee ◽  
Mohammad Al-Daydammony
Keyword(s):  
Sodium Excretion ◽  
Refractory Hypertension ◽  
Fractional Sodium Excretion

scholarly journals Presentation of the Child with Renal Disease and Guidelines for Referral to the Pediatric Nephrologist

2012 ◽  
Vol 2012 ◽  
pp. 1-5 ◽  
Author(s):  
Amin J. Barakat
Keyword(s):  
Urinary Tract ◽  
Renal Disease ◽  
Systemic Disease ◽  
Renal Involvement ◽  
Signs And Symptoms ◽  
Pediatric Nephrologist ◽  
Modes Of Presentation ◽  
Renal Tubular ◽  
High Index Of Suspicion

Renal disease is a major cause of morbidity and mortality. Pediatric patients with renal disease, especially younger ones may present with nonspecific signs and symptoms unrelated to the urinary tract. Pediatricians, therefore, should be familiar with the modes of presentation of renal disease and should have a high index of suspicion of these conditions. Affected patients may present with signs and symptoms of the disease, abnormal urinalysis, urinary tract infection, electrolyte and acid-base abnormalities, decreased renal function, renal involvement in systemic disease, glomerular and renal tubular diseases, congenital abnormalities, and hypertension. Pediatricians may initiate evaluation of renal disease to the extent that they feel comfortable with. The role of the pediatrician in the management of the child with renal disease and guidelines for patient referral to the pediatric nephrologist are presented.

Role of the renal kinin-prostaglandin system in diltiazem-induced natriuresis

1986 ◽  
Vol 250 (2) ◽  
pp. F197-F202
Author(s):  
M. Seino ◽  
K. Abe ◽  
N. Nushiro ◽  
K. Omata ◽  
K. Sato ◽  
...  
Keyword(s):  
Urinary Excretion ◽  
Significant Relationship ◽  
Intravenous Infusion ◽  
Renal Hemodynamics ◽  
Prostaglandin E ◽  
Drug Induced ◽  
Entry Blocker ◽  
Prostaglandin System

Intravenous infusion of the Ca2+ entry blocker diltiazem (10 micrograms . kg-1 . min-1 for 30 min) induced an increase in urinary excretion of sodium (UNaV) from 209 +/- 42 to 922 +/- 311 mueq without significant alterations in renal hemodynamics in anesthetized rabbits. Urinary excretion of kinin (UkinV) and prostaglandin E (UPGEV) were also increased by diltiazem, from 14.3 +/- 2.5 to 25.9 +/- 4.8 ng and 1.33 +/- 0.20 to 2.44 +/- 0.34 ng, respectively. Moreover, there was a significant correlation between UkinV and UNaV (r = 0.81, P less than 0.05). A significant relationship between UPGEV and UNaV (r = 0.83, P less than 0.05) was also observed. However, no correlation between urinary excretion of kallikrein (UkallV) and UNaV was found after infusion of diltiazem. Further, to examine a possible contribution of renal kinins and prostaglandins in diltiazem-induced natriuresis, aprotinin (50,000 KIU/kg bolus + 1,000 KIU . kg-1 . min-1 infusion) and indomethacin (8 mg/kg) were used. Aprotinin pretreatment attenuated diltiazem-induced natriuresis, accompanied by suppression of UkallV, UkinV, and UPGEV. However, indomethacin pretreatment did not affect this drug-induced natriuresis, although UPGEV was significantly decreased. Furthermore, under the indomethacin pretreatment, a significant increase in UkinV was produced by diltiazem. These results suggest that renal kinins rather than renal prostaglandin E, at least in part, play a role in diltiazem-induced natriuresis.

Role of Renal Prostaglandin E2 in Chronic Renal Disease Hypertension

Nephron ◽  
1982 ◽  
Vol 32 (3) ◽  
pp. 202-206 ◽  
Author(s):  
L. Ruilope ◽  
Garcia Robles ◽  
C. Bernis ◽  
A. Barrientos ◽  
J. Alcazar ◽  
...  
Keyword(s):  
Renal Disease ◽  
Chronic Renal Disease ◽  
Prostaglandin E

scholarly journals Pathology and Epidemiology of Oxalate Nephrosis in Cheetahs

2017 ◽  
Vol 54 (6) ◽  
pp. 977-985 ◽  
Author(s):  
Emily P. Mitchell ◽  
Molly E. Church ◽  
Sarah M. Nemser ◽  
Betsy Jean Yakes ◽  
Eric R. Evans ◽  
...  
Keyword(s):  
Renal Disease ◽  
Interstitial Nephritis ◽  
Chronic Renal Disease ◽  
Renal Amyloidosis ◽  
Acinonyx Jubatus ◽  
Tubular Necrosis ◽  
Oxalate Crystals ◽  
Renal Tubular ◽  
Renal Tubular Necrosis

To investigate cases of acute oxalate nephrosis without evidence of ethylene glycol exposure, archived data and tissues from cheetahs ( Acinonyx jubatus) from North America ( n = 297), southern Africa ( n = 257), and France ( n = 40) were evaluated. Renal and gastrointestinal tract lesions were characterized in a subset of animals with ( n = 100) and without ( n = 165) oxalate crystals at death. Crystals were confirmed as calcium oxalate by Raman spectroscopy in 45 of 47 cheetahs tested. Crystals were present in cheetahs from 3.7 months to 15.9 years old. Cheetahs younger than 1.5 years were less likely to have oxalates than older cheetahs ( P = .034), but young cheetahs with oxalates had more oxalate crystals than older cheetahs ( P < .001). Cheetahs with oxalate crystals were more likely to have renal amyloidosis, interstitial nephritis, or colitis and less likely to have glomerular loop thickening or gastritis than those without oxalates. Crystal number was positively associated with renal tubular necrosis ( P ≤ .001), regeneration ( P = .015), and casts ( P ≤ .001) but inversely associated with glomerulosclerosis, renal amyloidosis, and interstitial nephritis. Crystal number was unrelated to the presence or absence of colitis and was lower in southern African than American and European animals ( P = .01). This study found no evidence that coexisting chronic renal disease (amyloidosis, interstitial nephritis, or glomerulosclerosis), veno-occlusive disease, gastritis, or enterocolitis contributed significantly to oxalate nephrosis. Oxalate-related renal disease should be considered as a potential cause of acute renal failure, especially in young captive cheetahs. The role of location, diet, stress, and genetic predisposition in the pathogenesis of oxalate nephrosis in cheetahs warrants further study.

Effects of Sevoflurane and Isoflurane on Renal Function and on Possible Markers of Nephrotoxicity 

1998 ◽  
Vol 89 (2) ◽  
pp. 307-322 ◽  
Author(s):  
Hideyuki Higuchi ◽  
Shinji Sumita ◽  
Hiroki Wada ◽  
Tatsuya Ura ◽  
Takeshi Ikemoto ◽  
...  
Keyword(s):  
Renal Function ◽  
Renal Disease ◽  
Urinary Excretion ◽  
Creatinine Clearance ◽  
Blood Urea Nitrogen ◽  
High Flow ◽  
Low Flow ◽  
Sevoflurane Anesthesia ◽  
Urea Nitrogen ◽  
Compound A

Background Low-flow sevoflurane anesthesia is associated with increasing circuit concentrations of compound A, which is nephrotoxic in rats, but the effect of compound A and low-flow sevoflurane anesthesia on renal function in humans is unclear. The authors compared the effects of high- and low-flow sevoflurane and isoflurane anesthesia on renal function and on several possible markers of nephrotoxicity in humans. Methods Forty-two patients without preexisting renal disease underwent either low-flow isoflurane (1 l/min, n = 14), low-flow sevoflurane (1 l/min, n 14), or high-flow sevoflurane (6 l/min, n = 14) anesthesia for body-surface-area surgery scheduled to last at least 4 h. Twenty-four-hour urinary excretion of N-acetyl-beta-glucosaminidase (NAG), beta2-microglobulin, protein, glucose, blood urea nitrogen (BUN), and serum creatinine concentrations were measured before and after anesthesia. Results There were no differences in blood urea nitrogen, creatinine, and creatinine clearance among the three groups after anesthesia. Increased urinary N-acetyl-beta-glucosaminidase excretions were seen in the low-flow and high-flow sevoflurane groups, but not in the low-flow isoflurane group (P &lt; 0.01). Ten patients in the low-flow sevoflurane group had 24-h urinary excretion of protein that exceeded the normal ranges after anesthesia, but only one patient in the isoflurane and none in the high-flow sevoflurane groups had this. Conclusions Low-flow sevoflurane anesthesia was associated with mild and transient proteinuria. However, the observed proteinuria was not associated with any changes in blood urea nitrogen, creatinine, and creatinine clearance in these patients with no preexisting renal disease.

The Blood and Urinary Clearance of 203Hg-Chlormerodrin in Renal Insufficiency

1972 ◽  
Vol 11 (01) ◽  
pp. 24-36
Author(s):  
J. S. Bajaj ◽  
R. C. Bhat ◽  
A. K. Basu ◽  
J. S. Guleria
Keyword(s):  
Renal Insufficiency ◽  
Renal Disease ◽  
Urinary Excretion ◽  
Creatinine Clearance ◽  
Blood Clearance ◽  
Endogenous Creatinine Clearance ◽  
Significant Difference ◽  
Two Parameters

SummaryStudies performed on patients with renal disease, with and without significant renal insufficiency, have shown a statistically significant difference in the blood clearance and urinary excretion of 203Hg-Chlormerodrin in these two groups. An attempt has been made to correlate these two parameters with the endogenous creatinine clearance.

Role of AQP1 in endotoxemia-induced acute kidney injury

2008 ◽  
Vol 294 (6) ◽  
pp. F1473-F1480 ◽  
Author(s):  
Weidong Wang ◽  
Chunling Li ◽  
Sandra N. Summer ◽  
Sandor Falk ◽  
Wei Wang ◽  
...  
Keyword(s):  
Acute Kidney Injury ◽  
Sodium Excretion ◽  
Kidney Injury ◽  
Urine Osmolality ◽  
Urinary Sodium Excretion ◽  
Tubular Injury ◽  
Fractional Sodium Excretion ◽  
Type 3

The effect of endotoxemia (lipopolysaccharide, 2.5 mg/kg ip) was investigated in aquaporin (AQP) 1 knockout (KO) compared with wild-type (WT) mice. At baseline, KO mice exhibited higher water intake (WI) and urine output (UO). After endotoxemia, WI and UO remained higher in the KO than WT mice, and urine osmolality was lower. The higher serum osmolality in AQP1-KO mice during endotoxemia was associated with higher AQP2 (133 ± 8 vs. 100 ± 3%, P < 0.01), AQP3 (140 ± 8 vs. 100 ± 4%, P < 0.001) and Na+-K+-2Cl− cotransporter type 2 (NKCC2; 152 ± 14 vs. 100 ± 15%, P < 0.05) expression than that in WT mice. These responses during endotoxemia in the AQP1-KO mice compared with WT were associated with lower glomerular filtration rate (GFR) (69 ± 8 vs. 96 ± 8 ml/min, P < 0.05) and renal blood flow (0.77 ± 0.1 vs. 1.01 ± 0.1 ml/min, P < 0.01). Urinary sodium excretion and fractional sodium excretion were higher in KO compared with WT mice in endotoxemia and were accompanied by more severe tubular injury. With water repletion and comparable serum osmolalities, GFR was still lower in KO (57 ± 13 vs. 120 ± 6 ml/min, P < 0.01) compared with WT during endotoxemia. The abundance of AQP2 and AQP3 protein in KO mice was not different from WT mice; however, NKCC2, Na+/H+ exchanger type 3, and fractional sodium excretion remained higher in KO compared with WT. Thus the polyuria in AQP1-KO mice does not protect against endotoxemia-induced acute kidney injury but rather absence of AQP1 predisposed to enhanced endotoximic renal injury.

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