Kidney failure
Kidney failure is a disease where the kidneys lose their ability to effectively filter the waste products in the blood less than 15 percent of their normal function. It may be either acute kidney failure which may come on quite suddenly and in some cases, may be reversed, or chronic kidney failure, which may come gradually and in many cases, become irreversible. Swelling of legs, weakness, vomiting, loss of appetite, and confusion also may be an accompanying feature. Complications of acute and chronic failure are uremia, volume overload, and hyperkalemia. Anemia, heart disease, or high blood pressure are also complications of chronic failure.
23 million individuals in the United States 11.5% of the adult population have chronic kidney disease and are at heightened risk for cardiovascular events and for progression to kidney failure. Comparable estimates of disease burden have been described globally.6 Despite the availability of proven therapies to benefit patients with progressive kidney disease these treatments also have the potential to harm and increase cost. Clinical decision-making in CKD is difficult because of the heterogeneity of kidney disease, disease progression variability, and the competing risk of cardiovascular death. Predicting risk accurately would allow individualized decision-making to initiate early and appropriate patient management.
Advice for patients
There is no widely accepted predictive tool for CKD progression thus, doctors have to make ad hoc judgments regarding the patients to be treated, risking delayed treatment in those who do indeed progress to kidney failure or unnecessary treatment in those who do not progress. The severity of CKD has been suggested to inform decision-making related to treatment. Severity is generally staged based on the degree of glomerular filtration rate calculated from serum creatinine. Using reporting estimated GFR when serum creatinine is known has raised the level of CKD awareness and nephrologist referrals, but estimated GFR alone is inadequate for clinical decision-making.
There is evidence from recent studies that albuminuria gives extra prognostic value in predicting progression to kidney failure. Other research has explored using estimated GFR and albuminuria as input into prediction models, with extra clinical and laboratory information, but these models are either specific for a certain kind of kidney disease or lack external validation. The perfect model to forecast progression would be precise easy to use and very generalizable across a range of patients with CKD in independent populations.
Risk for kidney patients
Employing data from 2 distinct CKD cohorts, the aim of our research was to create and externally validate a precise but straightforward prediction model for CKD progression. The aim was also to employ variables that are commonly measured in CKD patients to develop a model to predict progression to kidney failure that would be simple to apply in clinical practice. We were particularly interested in models based on information accessible to a clinical laboratory, allowing reporting of the risk of kidney failure with laboratory test results.
The global high incidence of chronic kidney disease and the marked increase in the incidence of patients with end-stage renal disease have prompted nephrologists to detect renal risk factors. Over the last few years, it has become clear that cigarette smoking, apart from its long-accepted carcinogenic actions and its harmful role as a promoter of cardiovascular disease CVD, is a significant independent renal risk factor.
Notwithstanding a large body of literature reporting an adverse effect of smoking on renal function, some key features of smoking caused renal injury are not well understood. While there are sufficient nonrenal indications against smoking making smoking an independent risk factor for kidney failure is necessary to enhance the target and motivation for quitting smoking among CKD patients and further raise awareness regarding this renal risk factor among nephrologists.
Causes of kidney failure
It is unclear whether the renal impact of smoking influences both genders equally. A high population-based survey of Australia involving 11,247 randomly selected participants discovered lifetime exposure to smoking was significantly related to men having stage 3 or greater CKD, whereas in women it was not. Nevertheless, other investigations have identified comparable effects of smoking on kidney failure risk in both genders.
Secondly, it is not certain if the smoking-related risk for kidney failure varies with the number of cigarettes smoked. Dose-response relations have only been established for surrogate endpoints such as decline in renal function and rate of urine albumin excretion. Thirdly, it is unknown how much smoking cessation decreases kidney failure risk. Few studies have addressed this subject, and information is derived from a limited population of diabetic mellitus patients, once more based on surrogate indicators of renal injury, that is no hard end points. General population-based data are not available at all.
Thus, the purpose of the current research was to explore how the aforementioned factors of smoking affect the risk of kidney failure in a large population-based cohort. Smoking susceptibility may vary among men and women, and it is also becoming increasingly evident that the excess risk induced by smoking may be seemingly attenuated in the elderly due to differential survivorship and competing risks in ever-smokers, a survival bias.
This effect is not limited to some cardiovascular risk factors,13 and various studies indicate that the genetic background is significant for the susceptibility of individual subjects to smoking-induced damage. Therefore, to prevent the occurrence of a survival bias in elderly smokers, we analyzed men and women <70 years and ≥70 years of age at study entry separately.
Scientist research in kidney failure
Intravascular hemolysis is common in patients with advanced cardiac valvular disease or following heart valve replacement with mechanical prostheses. While acute kidney injury and CKD are established complications in conditions characterized by repeated hemolysis hemoglobinuria nephropathy like paroxysmal nocturnal hemoglobinuria,2,6 a GFR reduction related to hemolysis due to cardiac valvular disease or prostheses is less established. We describe a patient with underlying CKD who experienced a reduction in kidney function due to hemolysis secondary to mitral valve repair and Cosgrove-Edwards annuloplasty band implantation.
The mechanism of intravascular hemolysis in patients with cardiac valvular disease or prosthetic device placement is mechanical due to turbulent blood flow and shear forces across the diseased valve or prostheses, where velocity and pressure are dynamically changing. In most instances, as in the current patient, valvular regurgitation is a salient feature and such regurgitant flow significantly enhances the rate at which cells are traumatized. In the current patient, mechanical destruction of erythrocytes most likely was compounded by tightening of the mitral valve region with the banding procedure, resulting in a more abrupt change in blood velocity that enhanced shear force across the valve region and resulted in erythrocyte fragmentation.
Treatment for kidney failure
Mechanical trauma to erythrocytes releases hemoglobin into plasma, where hemoglobin is suspended by haptoglobin, thus creating a haptoglobin-hemoglobin protein complex. This complex, however too large to be filtered by the glomerulus, is sectored up by the liver, spleen, and bone marrow reticuloendothelial cells and broken down.
Once plasma haptoglobin becomes saturated with hemoglobin complexes, free plasma hemoglobin breaks from its normal tetrameric globin structure to dimeric hemoglobin. Dimeric hemoglobin is filtered more readily by the glomerulus than
tetrameric hemoglobin, and following filtration, hemoglobin is taken up into proximal tubules via the megalin-tubulin receptor system on the apical surface of these cells.
Intracellular hemoglobin subsequently breaks up into heme and globin. The elevated intracellular concentrations of heme are cytotoxic.