Introduction: Sepsis, an extremely prevalent condition in the intensive care unit, is usually associated with organ dysfunction, which can affect heart and kidney. Objective: To determine whether the cardiac dysfunction and the Troponin I forecast the occurrence of acute renal failure in sepsis. Methods: Cardiac dysfunction was assessed by echocardiography and by the serum troponin I levels, and renal impairment by AKIN criteria and the need of dialysis. Twenty-nine patients with incident sepsis without previous cardiac or renal dysfunction were enrolled. Results and Discussion: Patients averaged 75.3 ± 17.3 years old and 55% were male. Median APACHE II severity score at ICU admission was 16 (9.7 - 24.2) and mortality rate in 30 days was 45%. On the fifth day, 59% had ventricular dysfunction. Troponin serum levels on day 1 in the affected patients were 1.02 ± 0.6 ng/mL compared with 0.23 ± 0.18 ng/mL in patients without heart dysfunction (p = 0.01). Eighteen out of 29 patients (62%) underwent renal replacement therapy (RRT) and the percent of patients with ventricular dysfunction who required dialysis was higher (94% vs. 16%, p = 0.0001). Values of troponin at day 1 were used to develop a ROC curve to determine their ability to predict the need of dialysis. The area under the curve was 0.89 and the cutoff value was 0.4 ng/mL. Conclusion: We found that an elevation in serum troponin levels, while guarding a relationship with ventricular dysfunction, can be a precious tool to predict the need for dialysis in sepsis patients.
<p>Diastolic heart failure (HF) is an important factor that increases mortality related to the cardiovascular system in patients with chronic kidney disease (CKD) whose extent of kidney function deterioration differs. As a non-invasive method to allow early assessment, the E/e’ ratio estimated by tissue Doppler imaging can predict mortality and cardiovascular events in CKD patients with diastolic dysfunction. The current study evaluated 15 patients with CKD and left ventricular hypertrophy (LVH), who were selected according to a previously published protocol. In the present study, we reported for the first time the improvement in diastolic parameters measured by echocardiography in CKD patients with resistant hypertension and left ventricular hypertrophy 6 months after renal sympathetic denervation (RSD). Our results suggest that RSD in this kind of patients seems to avoid the progression to diastolic HF.</p>
Effects of aldosterone receptor (AR) blockade with eplerenone (epl) on renal Na(+) excretion, arterial blood pressure, intra-adrenal and renal ANG II, and plasma aldosterone levels during ANG II-dependent hypertension were evaluated. Rats from one cohort (n = 10/group) 1) control, 2) control + epl (25 mg/day), 3) ANG II (60 ng/min), and 4) ANG II + epl were maintained in metabolic cages for 28 days for daily urine collections. Systolic blood pressure (SBP) was measured weekly by tail-cuff. In a second cohort (n = 12/group), daily SBP was measured by telemetry (n = 6 rats/group) 1) control, 2) ANG II, and 3) ANG II + epl. A diet containing epl (0.1%) was provided after 1 wk of ANG II infusion. Direct monitoring of BP by telemetry showed that epl delayed the onset of the increase in SBP by 2 days and slightly reduced SBP (186 +/- 6 vs. 177 +/- 8 mmHg). Epl transiently increased Na(+) excretion within 24 h of treatment in both normo- and hypertensive rats; however, balance was reestablished within 5 days suggesting that alternative mechanisms for conserving Na(+) are activated. Cortical alpha-epithelial Na(+) channel content (alpha-ENaC) was not altered after 21 days of epl treatment. Epl exacerbated the ANG II-mediated increases in intrarenal ANG II (226 +/- 16 vs. 365 +/- 38 fmol/g) and further increased intra-adrenal ANG II (3.9 +/- 0.3 vs. 8.2 +/- 0.9 fmol/mg) and aldosterone (255 +/- 55 vs. 710 +/- 87 pmol/mg) content. Exacerbation of intrarenal ANG II levels likely contributes to the maintenance of alpha-ENaC protein content and thus Na(+) reabsorption, which helps explain the ineffectiveness of AR blockade in reducing SBP in ANG II-infused models of hypertension.
Mammalian renal intercalated cells (ICs) are known for their role in acid secretion and acid- base regulation. Based on previously published data, we discussed the theoretical reasons behind the development of additional renal IC biology characteristics, tracing them back phylogenetically to the simplest animals and protozoa. ICs have the following additional functions or attributes: (1) they play immunological roles in protecting the kidneys against both infective and aseptic kidney damage; (2) they are energized by V-ATPases in a similar fashion to protozoa; (3) they possess a T-antigen that is common in embryonic and cancer cells, which confers invasiveness ability to those cells; and (4) they exhibit plasticity and the ability to regenerate other epithelial cells (i.e., they exhibit stem cell behavior). Renal ICs may derive from amoeboid cells sharing these characteristics that originated from an evolutionary line that includes protists, or even the Last Eukaryotic Common Ancestor (LECA). None. This is the full abstract presented at the American Physiology Summit 2024 meeting and is only available in HTML format. There are no additional versions or additional content available for this abstract. Physiology was not involved in the peer review process.
Twenty‐seven patients with resistant hypertension and chronic kidney disease were treated by renal sympathetic denervation (RSD) and followed for 12 months. Patients were retrospectively divided into controlled and uncontrolled blood pressure (BP) groups. Increases in mean estimated glomerular filtration rate ( eGFR ) were found at months 1, 3, 6, and 12 in the controlled group ( P <.0001, for every time point). The mean change in eGFR after 12 months was 18.54±8.15 mL /min/1.73m 2 higher in the controlled group ( P =.0318). In patients in the controlled group with baseline eGFR <45 mL /min/1.73 m 2 , responders (with an increase in eGFR >6.2%) corresponded to 50% at 6 months and 83% at 12 months. In the patients with baseline eGFR ≥45 mL /min/1.73 m 2 , all patients were labeled as responders at months 6 and 12. Median albumin:creatinine ratio after 12 months was lower than baseline only in the controlled group ( P =.0003). Our results suggest that patients with this profile who reached BP control by RSD also experienced a significant improvement in renal function.