Development Of Kidney Function Research Articles

Prognosis for Type 1 Diabetes with Diabetic Nephropathy between 2000 and 2020 - Changes in Kidney Function Decline Over Time and Development of Cardiovascular Disease, Kidney Failure, and Mortality

IntroductionIndividuals with type 1 diabetes (T1D) and diabetic nephropathy (DN) experience progressive kidney function decline and high risk of cardiovascular disease (CVD) and mortality. This study explored changes in kidney function decline in new-onset DN between 2000-2020 and provided an updated prognosis for risk of kidney failure, CVD, and mortality. MethodsRegister-based cohort study in T1D with new-onset DN (severely increased albuminuria) between 2000-2020 at Steno Diabetes Center Copenhagen, Denmark. Data was derived from electronic health records and national registers. Kidney function development was expressed as trajectories of estimated glomerular filtration rate (eGFR) and measured GFR (mGFR) using mixed-effects models. The prognosis was presented in probabilities of developing complications, stratified by sex, prior CVD, and risk factor control by using simulations based on Poisson regression analysis. ResultsThe cohort comprised 591 individuals with median (IQR) age at DN onset of 53 (39-66) years and 57% were male. In 283 participants, mGFR were available. Plots of eGFR trajectories illustrated tendencies towards higher eGFR in more recent years, but this was not confirmed in mGFR trajectories. Poor risk factor control, prior CVD and male sex impacted mortality and morbidity rates negatively. For men/women with fair risk factor control and no prior CVD, the 10-year mortality rate from onset of DN was 28/26%. For men/women with poor risk factor control and CVD prior to DN onset, the 10-year-mortality rate was 62/62%. ConclusionThe results do not support an improved prognosis for T1D and DN, emphasizing the urgent need for new therapeutic approaches.

Cardiovascular and kidney outcomes of uric acid-lowering therapy in patients with different kidney functions: study protocol for a systematic review, pairwise and network meta-analysis

IntroductionHyperuricaemia has been implicated in the development of kidney function in populations with chronic kidney disease; however, the benefits of urate-lowering therapy (ULT) remain uncertain in different clinical studies. The...

New kidney function tests: Renal functional reserve and furosemide stress test

Acute kidney injury (AKI) occurs in 30-50% of all intensive care patients. Renal replacement therapy (RRT) has to be initiated in 10-15%. The early in-hospital mortality is about 50%. Up to 20% of all survivors develop chronic kidney disease after intensive care discharge and progress to end-stage kidney disease within the next 10years. For timely initiation of prophylactic or therapeutic interventions, it is crucial to exactly determine the actual kidney function, i. e., glomerular filtration rate (GFR), and to gain insight into the further development of kidney function. Traditionally, renal function has been estimated using serum levels of creatinine or urea. Unfortunately, both are notoriously unreliable and insensitive in intensive care patients. CystatinC has fewer non-GFR determinants when compared to creatinine and is more sensitive and accurate to detect early decreases of GFR. At present, new functional tests are discussed, namely the furosemide stress test (FST) and renal functional reserve (RFR). The FST consists of an intravenous infusion of 1.0-1.5 mg/kgBW furosemide to critically ill patients with AKI. An increase in urine output to >100 ml/h is indicative of aGFR >20 ml/min and almost certainly excludes progression to AKI stage III and need for RRT. Estimation of RFR can be made by short-term oral or intravenous administration of ahigh protein load. Asubsequent increase in GFR defines the presence and the magnitude of functional reserve which can be activated. Loss of RFR is an indicator of loss of functioning nephron mass and incomplete recovery following AKI. Both FST and RFR can help to improve diagnosis and care of high-risk patients with acute and chronic kidney disease.

189 THE PRESENCE OF HEMOLYTIC SPUR CELL-ANEMIA STRONGLY AFFECTS SURVIVAL IN PATIENTS WITH LIVER CIRRHOSIS

GFR of 61ml/min and showed an improvement of kidney function at year 1 (mean GFR 69ml/min), which was maintained over the 3 years. Comparing baseline characteristics of the respective groups, short cold ischemia time, lower age and short ICU stay were associated with a better development of kidney function. In a multivariable clinical prediction model we found predicted probabilities for GFR very close to observed probabilities for development of CKD 3 or worse. However, prediction of CKD 4 or 5 was less accurate. Conclusions: Imputing the classical risk factors in a prediction model leads to a good prediction of loss of kidney function, but cannot predict whether a patient will later require dialysis. The recognized patterns further underline that liver recipients are a very heterogeneous group and that even a deterioration of kidney function in the first post transplant year does not predict if it later recovers or not.

CBP and p300 in renin homeostasis: can they drive the fate?

CBP and p300 in renin homeostasis: can they drive the fate?

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

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 N(G)-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.

Effects of Prenatally Administered Thyroid Hormones or Glucocorticoids on Maturation of Kidney Function in Newborn Rats

Influences of treatment with thyroid hormones or dexamethasone during pregnancy on development of kidney function were studied in newborn rats. Treatment of dams for 3 days is followed by a higher rate of urine production in newborn rats. A statistically significant raise of sodium/potassium ratio in tetraiodothyronine- or dexamethasone-treated rats indicates a higher degree of maturation of kidney function. Treatment of dams with dexamethasone is followed by an increase of absolute excreted quantities of sodium and potassium in newborn rats. Treatment of dams with triiodothyronine can increase renal excretion of p-aminohippurate in newborn rats.