Glomeruli are far more permeable to H2O and salt than other capillaries.

The formation of plasma ultrafiltrate depends upon high hydrostatic pressure and permeability of the glomeruli

Aldosterone is released when afferent arterial pressure falls

Antidiuretic hormone (ADH) is released when plasma osmolality becomes too high.

The collecting tubule reabsorbs sodium and secretes potassium in response to aldosterone, and is permeable to H2O only in the presence of ADH

The thick ascending limb is permeable to salt, but not to H2O or urea.

The tubules are able to concentrate the filtrate because the descending limb is highly permeable to H2O and urea but not to salt, and the ascending limb is permeable to salt. Salt leaving the ascending limb creates a hypertonic interstitium that forces H2O from the descending limb

Renin is released in response to low hydrostatic pressure in the afferent arteriole, which stimulates the juxtaglomerular cells

ADH is released by the posterior pituitary in response to high plasma osmolality

Sodium is a threshold substance, meaning that no sodium will be excreted in the urine until the renal threshold (a plasma sodium concentration of approximately 120 mmol/L) is exceeded

Potassium is not a threshold substance and will be secreted by the tubules even when plasma potassium levels are low

Patients on diuretics or who have hypovolemia become hypokalemic for this reason

Some substances (e.g., penicillin) can be excreted at a rate exceeding glomerular filtration because the tubules secrete them. The tubules are responsible for concentrating the filtrate in conditions of water deprivation and diluting it in conditions of water excess.

When tubular function is lost, salt and water equilibrate by passive diffusion and the specific gravity of the urine becomes the same as the plasma, approximately 1.010

Urine specimens should be plated and incubated within 2 hours of collection (some labs use a 1-hour time limit), and within 24 hours if the sample is refrigerated at 2°C–8°C immediately following collection. No additives are permitted when urine is collected for culture.

Sample collection for routine urinalysis in the first morning voided sample is the most sensitive for screening purposes because formed elements are concentrated, but random samples are satisfactory because glomerular bleeding, albuminuria, and cast formation may occur at any time. Preservative tablets should be avoided because they may cause chemical interference with some dry reagent strip and turbid metric protein tests. Changes in glucose, bilirubin, and urobilinogen can occur within 30 minutes of collection. Therefore, samples should be refrigerated if not tested within 2 hours

Pigment-producing substance causes deep yellow urine and yellow foam with bilirubin

Homogentisic acid causes dark brown or black-colored urine.

Myoglobin causes a red to red-brown color in urine, and biliverdin causes a green or yellow-green color.

In addition to metabolic diseases and renal disease, abnormal color can be caused by drugs (e.g., Gantrisin), dyes excreted by the kidneys (e.g., PSP), and natural or artificial food coloring (e.g., beets).

In the lead poisoning normal urine color but produces red

fluorescence when urine is examined with an ultraviolet (Wood’s) lamp normal urine color but produces red fluorescence when urine is examined with an ultraviolet (Wood’s) lamp

Lead poisoning blocks the synthesis of heme, causing accumulation of PBG and coproporphyrin III in urine. However, uroporphyrin levels are not sufficiently elevated to cause red pigmentation of the urine.There is sufficient coproporphyrin to cause a positive test for fluorescence.

Thanks Dr. Moaed

Segun las guias KDIGO se debe estimar el filtrado glomerular usando fórmulas cómo CLD-EPI o MDRD y para un mejor resultado en etapas iniciales se puede implementar la fórmula de CLD-EPI cystatin

Sorry  it's CKD-EPI

CKD is an important Non communicable disease & is a chronic irreversible renal disease . it is diagnosed by eGFR ( utilizing serum creatinine ) & Proteinuria , While AKI is diagnosed by serum creatinine & urine output . CKD is classified on the basis of GFR using ' CKD-EPI calculator ' utilizing race , sex & age . Stages 1-3 are mild to moderate CKD , stage 4 is severe CKD & stage 5 is end stage renal failure . Early diagnosis is made by primary & secondary care doctors in stages 1- 3 . Stage 4-5 are managed by Nephrologists . The basis of this classification is to bring uniformity in diagnosis of CKD . Early diagnosis & management will delay progression of CKD to severe stages .

According to KDOQI Guideliness one uses GFR to categorize the stages of CKD. Please see table below and consult the site.

http://www2.kidney.org/professionals/kdoqi/guidelines_ckd/p4_class_g1.htm

CKD is now one of the major public health problems . In 2002, CKD was defined by the National Kidney Foundation Kidney Disease Outcomes Quality Initiative (K/DOQI) as the presence of reduced kidney function, or kidney damage, for a period of 3 months or greater . The 2012 Kidney Disease, Improving Global Outcomes (KDIGO) Guidelines for the evaluation and management of CKD by GFR (G1-5) G1 Normal or high ≥ 90 but with active urinary sediment, G2 mildly decreased 60-89, G3a mildly to moderately decreased 45-59, G3b moderately to severely decreased 30-44, G4 severely decreased 15-29 and G5 Kidney failure

Hello CKD-EPI IS THE BEST OPTION. Maybe this can help you!

Montañés Bermúdez, R., Bover Sanjuán, J., Oliver Samper, A., Ballarín Castán, J. A., & Gràcia García, S. (2010). [Assessment of the new CKD-EPI equation to estímate the glomerular filtration rate]. Nefrologia: Publicacion Oficial De La Sociedad Española Nefrologia, 30(2), 185–194. https://doi.org/10.3265/Nefrologia.pre2009.Dic.5838

eGFR is the basis for the classification of chronic kidney disease?How.

A simple question and a very difficult answer. For example:

The Killip Classification is frequently used during acute myocardial infarction. First published in 1967, this system focuses on physical examination and the development of heart failure to predict risk. Only 250 patients...

For 50 years, no one came up with a better classification.

The best method to evaluate the GFR is inulin depuration and, in second cystatin C depuration. The formula of CKD-EPI cys C is the best

The level of GFR should be estimated from prediction equations that take into account the serume creatinine concentration and variables such as age, gender, or weight, or by measurement of creatinine clearance using timed (for example, 24 hours) urine collection. https://www.kidney.org/sites/default/files/docs/ckd_evaluation_classification_stratification.pdf Guideline 4, p 81

@ Olena Polyakova ,

It ranges from Stage 3 to 4 . More data is required regarding this GFR of 49 - 15 . Is it a single or multiple samples ? If multiple , is it at the same time or done at different times in the same patient ?

This suggests that the patient has AKI on CKD . CKD is an irreversible & chronic disease & improvement in GFR suggests AKI on CKD . Has the patient recovered with steroids ?

At an eGFR of 49 , I would diagnose this as CKD Stage 3 . The further decline is due to AKI , which can be measured by rise in serum creatinine ( by utilizing KDIGO AKI criteria ) . eGFR is only for assessing severity of CKD .

CKD EPI Equation more useful in patients compare to other formulas. Because if we talk about results calculations by other like CG, MDRD - a lot of differences.

I agree with Michaela.

Classification of CKD is using GFR and also albumine to creatinine ratio.

according to GFR we can classify CKD to mild and moderate and severe through the albumin/creatinine ratio