Jumat, 23 Juni 2023

Kidney Characteristic Gfr

Kidney Characteristic Gfr

The best overall indicator of the glomerular function is the glomerular filtration rate (GFR). GFR is the rate in milliliters per minute at which substances in plasma are filtered through the glomerulus; in other words, the clearance of a substance from the blood. The normal GFR for an adult male is 90 to 120 mL per minute. The characteristics of an ideal marker of GFR are as follows: 

Creatinine is the by-product of creatine phosphate in muscle, and it is produced at a constant rate by the body. For the most part, creatinine is cleared from the blood entirely by the kidney. Decreased clearance by the kidney results in increased blood creatinine. The amount of creatinine produced per day depends on muscle bulk. Thus, there is a difference in creatinine ranges between males and females with lower creatinine values in children and those with decreased muscle bulk. Diet also influences creatinine values. Creatinine can change as much as 30% after the ingestion of red meat. As GFR increases in pregnancy, lower creatinine values are found in pregnancy. Additionally, serum creatinine is a later indicator of renal impairment-renal function is decreased by 50% before a rise in serum creatinine is observed. Serum creatinine is also utilized in GFR estimating equations such as the Modified Diet in Renal Disease (MDRD) and the CKD-EPI (Chronic Kidney Disease Epidemiology Collaboration) equation. These eGFR equations are superior to serum creatinine alone since they include race, age, and gender variables. GFR is classified into the following stages based on kidney disease (Gounden, 2021).

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Estimated GFR (eGFR) is a key method for identifying people with chronic kidney disease (CKD). eGFR is calculated using the Modification of Diet in Renal Disease (MDRD) Study equation or the CKD-EPI equation provides a more clinically useful measure of kidney function than serum* creatinine alone. This equation takes into account several factors that impact creatinine production, including age, gender, and race.

Definition And Classification Of Chronic Kidney Disease: A Position Statement From Kidney Disease: Improving Global Outcomes (kdigo)

GFR = 141 × min (S/κ, 1) × max (S/κ, 1) × 0.993 × 1.018 [if female] × 1.159 [if black] Abbreviations/unitsS is serum creatinine in mg/dL, κ = 0.7 for females and 0.9 for males, α = -0.329 for females and -0.411 for males, min = the minimum of S/κ or 1, andmax = the maximum of S/κ or 1All articles published by are made immediately available worldwide under an open access license. No special permission is required to reuse all or part of the article published by , including figures and tables. For articles published under an open access Creative Common CC BY license, any part of the article may be reused without permission provided that the original article is clearly cited. For more information, please refer to https:///openaccess.

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Baseline

Glomerular Filtration (glomerulus)

Department of Medicine, Division of Nephrology, Medical University of South Carolina, 96 Jonathan Lucas Street, MSC 629, CSB 822, Charleston, SC 29425, USA

Chronic kidney disease (CKD) is generally regarded as a final common pathway of several renal diseases, often leading to end-stage kidney disease (ESKD) and a need for renal replacement therapy. Estimated GFR (eGFR) has been used to predict this outcome recognizing its robust association with renal disease progression and the eventual need for dialysis in large, mainly cross-sectional epidemiological studies. However, GFR is implicitly limited as follows: (1) GFR reflects only one of the many physiological functions of the kidney; (2) it is dependent on several non-renal factors; (3) it has intrinsic variability that is a function of dietary intake, fluid and cardiovascular status, and blood pressure especially with impaired autoregulation or medication use; (4) it has been shown to change with age with a unique non-linear pattern; and (5) eGFR may not correlate with GFR in certain conditions and disease states. Yet, many clinicians, especially our non-nephrologist colleagues, tend to regard eGFR obtained from a simple laboratory test as both a valid reflection of renal function and a reliable diagnostic tool in establishing the diagnosis of CKD. What is the validity of these beliefs? This review will critically reassess the limitations of such single-focused attention, with a particular focus on inter-individual variability. What does science actually tell us about the usefulness of eGFR in diagnosing CKD?

Toxins

Key Contribution: This banner paper for this Special Edition of Toxins reviews and assess the implicit limitations of using eGFR snapshots for CKD diagnosis; a comprehensive approach to establish individual risk profile in CKD patients including age, eGFR slope, proteinuria, GFR variability, nutritional and metabolic profile suggested.

Pdf] Reporting Of Estimated Glomerular Filtration Rate: Effect On Physician Recognition Of Chronic Kidney Disease And Prescribing Practices For Elderly Hospitalized Patients.

Glomerular filtration rate (GFR) was originally introduced to estimate glomerular function by calculating the amount of fluid filtered through the renal glomeruli per unit of time. It is not a measure of single-nephron glomerular function; rather, it is a measure reflecting the summation of the filtration of all glomerular capillaries in the human kidney [1]. When a solute is freely filtered through the glomeruli and is neither reabsorbed nor secreted by tubules, as in the case of inulin, then the clearance of that solute may be used to measure GFR. Thus, GFR has been determined by finding the volume of blood glomeruli clear of insulin per minute and is calculated by the formula urine concentration times urine flow per plasma concentration [2, 3]. In clinical practice, creatinine is substituted for inulin as creatinine is present naturally in the body so it does not need to be injected like inulin [4, 5]. However, creatinine is not an ideal marker for estimating GFR due to its tubular secretion that increases through the course of renal disease; the more advanced the disease the larger the ratio of secreted to freely filtered creatinine [6]. In addition, creatinine being a waste product of protein metabolism in muscles, one must assume that creatinine clearance as a true reflection of intrinsic renal pathology may theoretically depend on the condition of a steady state with a constant and stable generation of creatinine in the muscle unaffected by catabolism (1), no changes in muscle activity (2), or dietary influences (3). It may also be assumed that creatinine should have a stable distribution with a relatively constant concentration in the serum (4) and adequate delivery to the glomerular capillaries using the so-called one compartment model (5) necessitating stable cardiovascular status and good vascular supply to the kidneys with the absence of acute changes in cardiac output or hydration status, current administration of non-steroid anti-inflammatory drugs (NSAID) or of any other medication acutely affecting renal blood flow (RBF) including blood pressure lowering agents, especially angiotensin converting enzyme (ACE) inhibitors or angiotensin II type 1 receptor blockers (ARBs). Functionally, the human kidneys can be simplified into two conceptual compartments—one of a filter and the other one the repressor; however, it is only the latter one that is energy expensive in terms of O

Characteristics

It is important to recognize that creatinine clearance as a reflection of decreased filtration due to actual renal disease is dependent on all these assumptions and that especially if the autoregulation of the afferent arterioles is affected by chronic disease such as diabetes mellitus, hypertension, congestive heart failure, or many others [7, 8], creatinine clearance will be highly variable creating a snapshot effect should creatinine clearance be measured, like in many studies, only a few times a year.

1.2. The Concept of the Estimation of Glomerular Filtration Rate by Estimating the Clearance of a Marker: The Estimation of an Estimation

General

Chronic Kidney Disease (ckd)

Since the calculation of creatinine clearance by a 24-hour urine collection has been cumbersome and is subject to much imprecision during collection, mGFR (measured GFR) as measured by urine collection of filtered creatinine has been largely replaced by eGFR, derived from approximations obtained through large epidemiological studies establishing correlations between serum creatinine and mGFR as influenced by parameters known to modify this relationship including age, sex, race, and others [9, 10, 11]. One such formula is CKD-EPI [12, 13], which was obtained from large cross-sectional studies of patients with or without renal disease where correlation between serum creatinine values and mGFR as measured by clearance of exogenous filtration markers such as iothalamate has been established using the formula GFR = 141 × min (S

× 1.018 (if female) × 1.159 (if black), accounting for variables of age, sex, and race (black vs. non-black). Yet, in the study populations used for establishing this formula, the elderly, especially subjects above 65 years of age, black subjects, and patients with an actual diagnosis of CKD were largely under-represented [12]. Furthermore, the equation obtained is based on a population-based average ignoring such

Evaluation

Glomerular filtration rate (GFR) was originally introduced to estimate glomerular function by calculating the amount of fluid filtered through the renal glomeruli per unit of time. It is not a measure of single-nephron glomerular function; rather, it is a measure reflecting the summation of the filtration of all glomerular capillaries in the human kidney [1]. When a solute is freely filtered through the glomeruli and is neither reabsorbed nor secreted by tubules, as in the case of inulin, then the clearance of that solute may be used to measure GFR. Thus, GFR has been determined by finding the volume of blood glomeruli clear of insulin per minute and is calculated by the formula urine concentration times urine flow per plasma concentration [2, 3]. In clinical practice, creatinine is substituted for inulin as creatinine is present naturally in the body so it does not need to be injected like inulin [4, 5]. However, creatinine is not an ideal marker for estimating GFR due to its tubular secretion that increases through the course of renal disease; the more advanced the disease the larger the ratio of secreted to freely filtered creatinine [6]. In addition, creatinine being a waste product of protein metabolism in muscles, one must assume that creatinine clearance as a true reflection of intrinsic renal pathology may theoretically depend on the condition of a steady state with a constant and stable generation of creatinine in the muscle unaffected by catabolism (1), no changes in muscle activity (2), or dietary influences (3). It may also be assumed that creatinine should have a stable distribution with a relatively constant concentration in the serum (4) and adequate delivery to the glomerular capillaries using the so-called one compartment model (5) necessitating stable cardiovascular status and good vascular supply to the kidneys with the absence of acute changes in cardiac output or hydration status, current administration of non-steroid anti-inflammatory drugs (NSAID) or of any other medication acutely affecting renal blood flow (RBF) including blood pressure lowering agents, especially angiotensin converting enzyme (ACE) inhibitors or angiotensin II type 1 receptor blockers (ARBs). Functionally, the human kidneys can be simplified into two conceptual compartments—one of a filter and the other one the repressor; however, it is only the latter one that is energy expensive in terms of O

Characteristics

It is important to recognize that creatinine clearance as a reflection of decreased filtration due to actual renal disease is dependent on all these assumptions and that especially if the autoregulation of the afferent arterioles is affected by chronic disease such as diabetes mellitus, hypertension, congestive heart failure, or many others [7, 8], creatinine clearance will be highly variable creating a snapshot effect should creatinine clearance be measured, like in many studies, only a few times a year.

1.2. The Concept of the Estimation of Glomerular Filtration Rate by Estimating the Clearance of a Marker: The Estimation of an Estimation

General

Chronic Kidney Disease (ckd)

Since the calculation of creatinine clearance by a 24-hour urine collection has been cumbersome and is subject to much imprecision during collection, mGFR (measured GFR) as measured by urine collection of filtered creatinine has been largely replaced by eGFR, derived from approximations obtained through large epidemiological studies establishing correlations between serum creatinine and mGFR as influenced by parameters known to modify this relationship including age, sex, race, and others [9, 10, 11]. One such formula is CKD-EPI [12, 13], which was obtained from large cross-sectional studies of patients with or without renal disease where correlation between serum creatinine values and mGFR as measured by clearance of exogenous filtration markers such as iothalamate has been established using the formula GFR = 141 × min (S

× 1.018 (if female) × 1.159 (if black), accounting for variables of age, sex, and race (black vs. non-black). Yet, in the study populations used for establishing this formula, the elderly, especially subjects above 65 years of age, black subjects, and patients with an actual diagnosis of CKD were largely under-represented [12]. Furthermore, the equation obtained is based on a population-based average ignoring such

Evaluation

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