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admin | Natural Weight Loss Supplement | 09.06.2014
Second, I wanted to post these for anyone else that may see high levels on their bloodwork. Other factors that can falsely increase serum creatinine also need to be taking into consideration that will change the range value of eGFR, such as certain medications ie; ACE inhibitors, certain antibiotics and hydration status. Cystatin C is another blood test that is used on renal function, that has no influence on one's muscle mass, protein intake or physical activity. The excretory function of the kidney serves to rid the body of undesirable end products of metabolism. The two most popular screening tests for renal function are serum urea nitrogen and serum creatinine.
Historically, urea was reported as blood urea nitrogen (BUN) and this terminology has been incorrectly carried over to the present. Urea is filtered by the glomeruli; however, about 40-70% (amount depends on urine flow) is reabsorbed by passive diffusion into blood across the renal tubular epithelium. SUN is not a sensitive indicator of renal dysfunction because renal function must be reduced by more than 50% to result in a rise of SUN. Patients with hepatic disease, muscular dystrophy, paraplegia and poliomyelitis may excrete less creatinine due to decreased production. Note: Creatinine production is based on weight and gender that is generally related to muscle mass. A useful assessment of renal function is the measurement of the glomerular filtration rate (GFR), especially in older people.
Since creatinine clearance is related to patient size, a more accurate formula includes an estimation of body surface area in square meters obtained from a nomogram using the height and weight of the patient.
The relationship between serum creatinine and creatinine clearance is logarithmic (see Figure 1). The endogenous creatinine clearance rate is primarily an estimate of GFR; however, a small amount of tubular secretion augments glomerular filtration. An alternative to measuring GFR is to use the Cockroft and Gault equation[1] to estimate creatinine clearance based on a single measurement of serum creatinine.
The most often used function tests are renal concentrating power and the ability to produce an acid urine (in suspected renal tubular acidosis). Random testing of either specific gravity or osmolality is not very informative, due to the effect of fluid intake.
The ratio is increased in conditions in which there is increased urea synthesis, as observed in the presence of blood in the GI tract, in muscle wasting disease, and in severe tissue trauma, all of which provide proteins that are catabolized into their constituent amino acids, which are then deaminated and converted into urea. Decreased ratios are seen in the presence of decreased urea synthesis (chronic glomerulonephritis with protein deficiency, severe hepatic insufficiency, and starvation) and decreased urea reabsorption (overhydration and rapid hydration). Acute renal failure occurs rapidly and is potentially reversible if the initial illness or insult is survived (60% survival rate).
Acute diffuse inflammatory changes in the glomeruli with hematuria, RBC casts, mild proteinuria, and often hypertension, edema, and azotemia. The ratio of the clearances of a high and a low molecular weight protein (IgG and albumin, respectively) gives an indication of the nature of glomerular damage in glomerular proteinuria (selective vs.
The routine urinalysis is carried out in three phases: macroscopic, chemical, and microscopic analysis. These are the result of progressive degenerative changes occurring in cellular casts and they are associated with severe chronic renal disease and amyloidosis. These casts are probably due to leakage of lipoproteins through the glomerular filter and are associated with nephrotic syndrome, diabetes mellitus, and damaged renal tubular epithelial cells.
A 49-year-old AIDS patient with multiple drug-resistant HIV gets tenofovir added to his drug regimen. Six weeks after starting tenofovir the patient was brought to the emergency department with a 4-day history of progressive fatigue, weakness, confusion, oliguria, and myalgia. An 87-year-old retired tailor appears in his physician’s office complaining of the slow onset of ankle and shin swelling, mild shortness of breath, and fatigue.

Lab tests often provide the initial recognition of renal impairment and can be used to direct further therapy. Thus, in conditions in which the glomerular filtration rate is decreased, SUN will be increased. Thus, this measurement can be used to assess the relative completeness of a 24-hour urine collection.
It should be noted that many laboratories use alkaline picrate (Jaffe) method for measuring creatinine. Thus, be circumspect when treating individuals with a high normal creatinine when a low creatinine is appropriate due to small muscle mass. The inulin clearance rate closely approximates the true GFR since inulin is freely filtered by the glomerulus with minimal tubular absorption or secretion. Thus, initially, for small numeric changes in serum creatinine, there are significant numeric changes for creatinine clearance.
Relationship between serum creatinine, creatinine clearance and number of remaining nephrons. Therefore, total urinary creatinine is slightly higher than the amount actually filtered by the glomeruli. However, other conditions may also change the ratio, depending on the rate of urea synthesis, kidney blood flow, or glomerular filtration rate. Other conditions such as intraperitoneal extravasation of urine and urinary enteric fistulas lead to greater urea reabsorption. The decrease in ratio due to hemodialysis is caused by the more efficient dialysis of urea vs.
Chronic renal failure usually develops over years in an insidious manner leading to endstage renal disease requiring lifelong dialysis or renal transplant. The decreased oncotic pressure stimulates a compensatory increase in hepatic lipoprotein synthesis, and, thus, hyperlipidemia is often seen in this condition. Total globulin concentration may be normal, but ?2-globulins are increased (alpha-2 macroglobulin and low-density lipoprotein), and ?-globulins may be low (see serum protein section). They are formed in two ways, by precipitation and gelling of proteins in tubular fluid, and by clumping of cells in tubules. They enter the urine stream by ameboid movement through and between tubular epithelial cells and sometimes they cross the glomerular capillary lumen. Their presence points to a pathological process occurring in the kidney and affecting the tubular portion of the nephron (tubular damage). Three days after starting treatment with levofloxacin, the patient was admitted to the hospital with palpable purpura and erythematous skin lesions over the lower limbs and trunk, with a markedly diminished urine output. His medical history was also notable for adrenal insufficiency, hypogonadism, anemia, peripheral neuropathy, asthma, and large B cell lymphoma of the thoracic spine. Urinalysis performed in the office reveals marked proteinuria, and the patient is seen for further evaluation and work-up.
In therapeutics, knowledge of renal function is essential for recommending proper doses of prescription drugs. This is especially true in the aged, where serum creatinine measurements are less reliable due to decreasing muscle mass. Serum urea nitrogen (SUN) is normally ~45% of total NPN, but may be 80% of NPN in some disease states. Urea is synthesized mostly in the liver as a by-product of the deamination of amino acids arising from protein catabolism. For this reason, urea clearance tests are less informative than creatinine clearance tests and have been discontinued. In later stages of uremia, small numeric changes in the clearance are associated with significant changes in serum creatinine.
The amount of urinary creatinine derived from tubular secretion rises proportionally in renal failure with an increase in serum creatinine.

This compound is completely filtered by the glomeruli and is not secreted or reabsorbed by the tubules. Increased tubular reabsorption of urea occurs with decreased tubular flow as a result of dehydration, decreased cardiac output, or shock (= prerenal azotemia), or due to renal disease, such as early acute glomerulonephritis, malignant nephrosclerosis, or postrenal obstruction. The disease is characterized by diffuse sclerosis of glomeruli, loss of nephrons, and loss of protein into the urine. Increase in lipoproteins is also caused by loss of factors regulating lipoprotein synthesis.
Hence, serum protein electrophoresis typically demonstrates diminished albumin and elevated alpha-2 globulin fraction.
Excretion of numerous casts is seen in all renal diseases associated with benign essential hypertension, and nephrotic syndrome.
These casts are associated with diseases with leukocytic exudation and interstitial inflammation. Epithelial casts are associated with exposure to nephrotoxic agents and exposure to some viruses. Measuring the clearance of endogenous creatinine (clearance of creatinine produced by metabolic processes) is much more practical and convenient but less accurate.
Note the decrease in the number of nephrons with decrease of clearance and increase in serum creatinine.
With advancing renal failure and increase in serum creatinine, the tubular secretion proportionally increases up to 40-60%. However, this method requires a special laboratory equipped to handle and measure radioactive isotopes. A patient with polyuria due to chronic renal failure (CRF) is unable to produce either a dilute or a concentrated urine.
In acute tubular necrosis, urea and creatinine are equally and passively returned to the tubular blood.
In the nephrotic syndrome there is a loss of a variety of proteins, such as transferrin, cortisol-binding globulin, thyroxine-binding globulin, and some coagulation factors. The matrix of all casts is a specific mucoprotein common to all casts, namely Tamm-Horsfall protein. These casts are associated with acute glomerulonephritis (most common), lupus nephritis, Goodpasture’s syndrome, and subacute bacterial endocarditis (SBE). Bilirubin, aminotransferase enzymes, and alkaline phosphatase were normal; lactate dehydrogenase was also normal.
Creatinine, for the most part, is freely filtered; thus, clearance of endogenous creatinine is a reflection of GFR. Measurement of osmolality with an osmometer is more accurate, but also more difficult than specific gravity measurements. This finding suggests loss of tubular concentrating and diluting ability and is frequently a prelude to anuria. The classification of casts is based on appearance, physical properties, and type of cellular components. Normally, only small amounts (< 6%) are reabsorbed by the tubules and an equal amount may be secreted by the tubules. Cells within the matrix can degenerate into coarse and finely granular casts and to waxy casts.
With advanced renal failure creatinine clearance overestimates true GFR, which is because of the increased amount of creatinine in urine due to tubular secretion, which in turn is caused by the high concentration of creatinine in circulation.

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