Total body water distribution of creatinine and urea in nephrectomized dogs

Schloerb, Paul R.

doi:10.1152/ajplegacy.1960.199.4.661

Cited by 58 publications

(30 citation statements)

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“…24 -26 The shorter (1.5-hour) half-life of CyC compared with creatinine accounts for the more rapid rise and the earlier attainment of a new steady state. 27 CyC is distributed in the extracellular volume, 28 whereas sCr is distributed in the total body water, 29 a volume that is 3 times larger. Therefore, the half-life of creatinine compared with CyC will be 3 times longer, and the time to achieve a new steady state will increase proportionally, implying that sCr will rise more slowly.…”

Section: Serum Cyc As a Marker Of Ci-akimentioning

confidence: 99%

Cystatin C and Contrast-Induced Acute Kidney Injury

Briguori

Visconti

Rivera³

et al. 2010

Circulation

219

181

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Background-Cystatin C (CyC) is more sensitive than serum creatinine (sCr) to rapidly detect acute changes in renal function. Methods and Results-We measured CyC together with sCr in 410 consecutive patients with chronic kidney disease undergoing either coronary and/or peripheral angiography and/or angioplasty. sCr was assessed at baseline and 24 and 48 hours after contrast media exposure. CyC was assessed at baseline and at 24 hours. Major adverse events (including death of any cause and dialysis) at 12 months were assessed. At 48 hours after contrast media exposure, contrast-induced acute kidney injury (defined as a sCr increase Ն0.3 mg/dL) occurred in 34 patients (8.2%). A CyC increase concentration Ն10% at 24 hours after contrast media exposure was detected in 87 patients (21.2%). This was the best CyC cutoff for the early identification of patients at risk for contrast-induced acute kidney injury (negative predictive valueϭ100%; positive predictive valueϭ39.1%). According to the defined cutoffs (that is, increase in CyC Ն10% and sCr Ն0.3 mg/dL), major adverse events occurred in 16 of 297 patients (5.4%) without any cutoffs satisfied (group 1), in 9 of 49 patients (18.4%) with only a CyC increase Ն10% (group 2), and in 9 of 31 patients (29%) with both cutoffs satisfied (group 3). By logistic regression analysis, the independent predictors of major adverse events at 1 year were group 2 (odds ratioϭ2.52; 95% confidence interval,

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Section: Serum Cyc As a Marker Of Ci-akimentioning

confidence: 99%

Cystatin C and Contrast-Induced Acute Kidney Injury

Briguori

Visconti

Rivera³

et al. 2010

Circulation

219

181

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“…Creatinine Vd and production were measured using injection of a known amount of unlabeled creatinine, as previously reported in bilaterally nephrectomized dogs. 33 Creatinine (30 mg/kg) was injected intravenously at 14 h after surgery, and blood samples were collected before injection and 4 h later. Vd of creatinine in nephrectomized mice was calculated from the 4-h increase in serum creatinine in the vehicle-injected mice (n ϭ 6 to 8 per group).…”

Section: Measurement Of Vd and Creatinine Productionmentioning

confidence: 99%

Reduced Production of Creatinine Limits Its Use as Marker of Kidney Injury in Sepsis

Doi¹,

Yuen²,

Eisner³

et al. 2009

Journal of the American Society of Nephrology

333

192

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Serum creatinine is used clinically to detect and evaluate acute kidney injury (AKI) and chronic kidney disease (CKD), 1,2 although the limitations of serum creatinine for the early detection and accurate estimation of renal injury are widely known. In AKI, serum creatinine does not accurately reflect the GFR because the patient is not in steady state. 3 Furthermore, serum creatinine is also influenced by tubular creatinine secretion and by nonrenal factors such as muscle mass, liver function, and nonrenal (gastrointestinal) elimination.Sepsis remains a serious problem in critically ill patients, and mortality from sepsis is increased dramatically when complicated by AKI; therefore, early detection and accurate evaluation of AKI is important in patients with sepsis. We modified the cecal ligation and puncture (CLP) mouse sepsis model to make it more clinically relevant, and our model developed sepsis-induced AKI. 4 -6 We found that serum creatinine increased to a lesser extent in CLP (approximately 0.5 mg/dl) than ischemia/reperfusion or cisplatin administration (Ͼ1 mg/dl) within 24 h of injury. To explore nonrenal factors that might account for this disparity, we used bilateral nephrectomy (BNx), a technique used recently by others to study the contribution of the kidney to cytokine metabolism and acute lung injury. 7 First, we evaluated sepsis in bilaterally nephrectomized mice. We induced sepsis by CLP surgery with 8-mm cecal ligation, which causes modest sublethal sepsis in normal outbred CD-1 mice. 8 All animals survived until they were killed at 18 h after surgery. CLP surgery in non-nephrectomized mice caused a numerically small, but not significant increase of serum creatinine (sham BNx ϩCLP group). As expected, we found large increases of serum creatinine in the BNxϩsham CLP group; however, induction of sepsis at the time of BNx significantly decreased serum creatinine (BNxϩCLP group) compared with nonseptic BNx alone (BNxϩsham CLP group; Figure 1A), raising doubt about whether serum creatinine accurately reflects impaired kidney function during sepsis. In contrast, nonrenal organ injury markers (aspartate aminotransferase [AST], alanine aminotransferase [ALT], and lactate dehydrogenase [LDH]) and serum TNF-␣ were higher in the BNxϩCLP group than in the BNxϩsham CLP group, confirming the presence of severe sepsis (Figure 1, ABSTRACTAlthough diagnosis and staging of acute kidney injury uses serum creatinine, acute changes in creatinine lag behind both renal injury and recovery. The risk for mortality increases when acute kidney injury accompanies sepsis; therefore, we sought to explore the limitations of serum creatinine in this setting. In mice, induction of sepsis by cecal ligation and puncture in bilaterally nephrectomized mice increased markers of nonrenal organ injury and serum TNF-␣. Serum creatinine, however, was significantly lower in septic animals than in animals subjected to bilateral nephrectomy and sham cecal ligation and puncture. Under these conditions treatment with chloroquine decrease...

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“…According to creatinine kinetics, it takes 5 h for creatinine to distribute evenly throughout all compartments 31,32 (plasma, remaining extracellular space, and intracellular space). Thus, 90-min values can be considerably higher than after 24 h. In other words, abrupt decrease in creatinine clearance may markedly raise plasma creatinine; however, this acute increase will level off and decrease with ongoing equilibration.…”

Section: Plasma Creatininementioning

confidence: 99%

Viscosity of Contrast Media Perturbs Renal Hemodynamics

Seeliger¹,

Flemming²,

Wronski³

et al. 2007

Journal of the American Society of Nephrology

145

132

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Contrast-induced nephropathy is a common cause of acute renal failure, and the mechanisms underlying this injury are not completely understood. We sought to determine how physicochemical properties of contrast media may contribute to kidney damage in rats. We administered contrast media of equivalent iodine concentrations but differing physiocochemical properties: the high-osmolality iopromide was compared to the high-viscosity iodixanol. In addition, the non-iodinated substances mannitol (equivalent osmolality to iopromide) and dextran (equivalent viscosity to iodixanol) were also studied. Both types of contrast media transiently increased renal and hindquarter blood flow. The high-osmolality agents iopromide and mannitol markedly increased urine production whereas iodixanol, which caused less diuresis, significantly enhanced urine viscosity. Only the high-viscosity agents iodixanol and dextran decreased renal medullary blood flux, erythrocyte concentration, and pO 2 . Moreover, iodixanol prolonged the tubuloglomerular feedback response and increased plasma creatinine levels to a greater extent than iopromide or dextran. Therefore, the viscosity of contrast media may play a significant role in contrast-induced nephropathy.

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Total body water distribution of creatinine and urea in nephrectomized dogs

Cited by 58 publications

References 0 publications

Cystatin C and Contrast-Induced Acute Kidney Injury

Cystatin C and Contrast-Induced Acute Kidney Injury

Reduced Production of Creatinine Limits Its Use as Marker of Kidney Injury in Sepsis

Viscosity of Contrast Media Perturbs Renal Hemodynamics

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