A camera-based method using Technetium-99m diethylenetriaminepentaacetic acid (Tc-99m DTPA) is commonly used to calculate glomerular filtration rate (GFR), especially, as it can easily calculate split renal function. Renal depth is the main factor affecting the measurement of GFR accuracy. This study aimed to compare the difference of renal depths between three formulae and a CT scan, and, additionally, to calculate the GFRs by four methods. We retrospectively reviewed the medical records of patients receiving a renal dynamic scan. All patients underwent a laboratory test within one month, and a computed tomography (CT) scan within two months, before or after the renal dynamic scan. The GFRs were calculated by employing a renal dynamic scan using renal depth measured in three formulae (Tonnesen’s, Itoh K’s, and Taylor’s), and a CT scan. The renal depths measured by the above four methods were compared, and the GFRs were compared to the modified estimated GFR (eGFR). Fifty-one patients were enrolled in the study. The mean modified eGFR was 60.5 ± 42.7 mL/min. The mean GFRs calculated by three formulae and CT were 45.3 ± 23.3, 54.7 ± 27.5, 56.5 ± 26.3, and 63.7 ± 30.0, respectively. All of them correlated well with the modified eGFR (r = 0.87, 0.87, 0.87, and 0.84, respectively). The Bland–Altman plot revealed good consistency between the calculated GFR by Tonnesen’s and the modified eGFR. The renal depths measured using the three formulae were smaller than those measured using the CT scan, and the right renal depth was always larger than the left. In patients with modified eGFR > 60 mL/min, the GFR calculated by CT was the closest to the modified eGFR. The Renal depth measured by CT scan is deeper than that using formula, and it influences the GFR calculated by Gate’s method. The GFR calculated by CT is more closely related to modified eGFR when modified eGFR > 60 mL/min.
The influence of chronic kidney disease (CKD) on the severity and prognosis of spontaneous intracerebral hemorrhage (ICH) has been scarcely investigated. We aimed to explore the association of admission estimated glomerular filtration rate (eGFR) levels with hemorrhagic stroke severity and outcomes in ICH patients.
Materials and methods
The patients enrolled in this study were from the China Stroke Center Alliance study (CSCA). Patients were divided into four groups according to differences in eGFR at admission (≥90; 60–89; 45–59; < 45). Multivariable logistic regression analysis was used to determine the association of the eGFR at admission with hemorrhagic stroke severity, in-hospital complications, discharge disposition, and in-hospital mortality after ICH.
A total of 85,167 patients with acute ICH were included in the analysis. Among them, 9493 (11.1%) had a baseline eGFR<60 ml/min/1.73 m2. A low eGFR was associated with an increased risk of in-hospital mortality [eGFR 60–89 ml/min/1.73 m2, odds ratio (OR) 1.36 (95% confidence interval (CI) 1.21–1.53); eGFR 45–59, 2.35 (1.97–2.82); eGFR<45, 4.18 (3.7–4.72); P for trend < 0.0001], non-routine discharge [eGFR 60–89, 1.11 (1.03–1.2); eGFR 45–59, 1.16 (1–1.35); eGFR<45, 1.37 (1.23–1.53); P for trend < 0.0001], hemorrhagic stroke severity [eGFR 60–89, 1 (0.95–1.05); eGFR 45–59, 1.39 (1.26–1.53); eGFR<45, 1.81 (1.67–1.96); P for trend < 0.0001], in-hospital complications of pneumonia [eGFR 60–89, 1.1 (1.05–1.14); eGFR 45–59, 1.3 (1.2–1.4); eGFR<45, 1.66 (1.57–1.76); P for trend < 0.0001] and hydrocephalus [eGFR 60–89, 0.99 (0.87–1.12); eGFR 45–59, 1.37 (1.1–1.7); eGFR<45, 1.54 (1.32–1.8); P for trend = 0.0139] after adjusting for confounding factors. With the decline in eGFR, the risk of hematoma evacuation increased in patients with an eGFR 45 to 59 ml/min/1.73 m2 (OR 1.48; 95% CI 1.37–1.61). No significant association between differences in eGFR at baseline and in-hospital complication of recurrent intracerebral hemorrhage was observed.
Low eGFR at baseline was associated with an increased risk of in-hospital mortality, non-routine discharge, hemorrhagic stroke severity and in-hospital complications such as pneumonia, hydrocephalus and hematoma evacuation in acute ICH patients.
Clinical studies have reported additive nephrotoxicity associated with the combination of vancomycin (VAN) and piperacillin-tazobactam (TZP). This study assessed differences in glomerular filtration rate (GFR) and urinary biomarkers between rats receiving VAN and those receiving VAN+TZP. Male Sprague-Dawley rats (n=26) were randomized to receive 96 hours of intravenous VAN at 150mg/kg/day, intraperitoneal TZP at 1400 mg/kg/day, or VAN+TZP. Kidney function was evaluated using fluorescein-isothiocyanate sinistrin and a transdermal sensor to estimate real-time glomerular filtration rate (GFR). Kidney injury was evaluated via urinary biomarkers including kidney injury molecule-1 (KIM-1), clusterin, and osteopontin. Compared to a saline control, only rats in the VAN group showed significant declines in GFR by day 4 (-0.39 mL/min/100 g body weight, 95% CI: -0.68 to -0.10, p=0.008). When the VAN+TZP and VAN alone treatment groups were compared, significantly higher urinary KIM-1 was observed in the VAN alone group on day 1 (18.4 ng, 95% CI: 1.4 to 35.3, p=0.03), day 2 (27.4 ng, 95% CI: 10.4 to 44.3, p=0.002), day 3 (18.8 ng, 95% CI: 1.9 to 35.8, p=0.03), and day 4 (23.2 ng, 95% CI: 6.3 to 40.2, p=0.007). KIM-1 was the urinary biomarker that most correlated with decreasing GFR on day 3 (Spearman’s rho: -0.45, p = 0.022) and day 4 (Spearman’s rho: -0.41, p = 0.036). Kidney function decline and increased KIM-1 were observed among rats that received VAN only, but not TZP or VAN+TZP. Addition of TZP to VAN does not worsen kidney function or injury in our translational rat model.
Phosphodiesterase V (PDEV) is upregulated in heart failure, leading to increased degradation of cGMP and impaired natriuresis. PDEV inhibition improves the renal response to B‐type natriuretic peptide in animal models. We tested the hypothesis that long‐term PDEV inhibition would improve renal function and cardiorenal response after short‐term volume load in subjects with pre–heart failure.
Methods and Results
A total of 20 subjects with pre–heart failure (defined as an ejection fraction ≤45% without previous diagnosis of heart failure) and renal impairment were randomized in a 2:1 manner to tadalafil or placebo. Baseline echocardiography and renal clearance study were performed, followed by a short‐term saline load and repeated echocardiography and renal clearance study. Subjects then received either tadalafil at a goal dose of 20 mg daily or placebo, and the study day was repeated after 12 weeks. Long‐term tadalafil did not improve glomerular filtration rate (median increase of 2.0 mL/min in the tadalafil group versus 13.5 mL/min in the placebo group;
=0.54). There was no difference in urinary sodium or cGMP excretion with PDEV inhibition following short‐term saline loading.
Glomerular filtration rate and urinary sodium/cGMP excretion were not significantly different after 12 weeks of tadalafil compared with placebo. These results do not support the use of PDEV inhibition to improve renal response in patients with pre–heart failure.
; Unique identifier: NCT01970176.