The kidneys regulate the volume and composition of extracellular fluid by producing urine. This process begins with the formation of an ultrafiltrate of plasma, which occurs as solutes, small proteins, and other non-cellular components of the blood pass through the glomerular filtration barrier. The volume of ultrafiltrate formed mainly depends on the number of functioning nephrons, though it is also influenced by the hydrostatic pressure within the glomerular capillary tuft. After filtration, the fluid’s composition is modified to meet the body’s physiological needs through the secretion and reabsorption of solutes and water as it moves along the nephron. In a healthy animal, under normal physiological conditions, less than 1% of the filtered fluid will be excreted as urine. Most frequently kidney disease is diagnosed when glomerular filtration rate (GFR) is decreased (usually recognized as azotemia), in a patient with either chronic kidney disease (CKD) or acute kidney injury (AKI).
Chronic kidney disease (CKD) is typically defined as a condition that persists for a specified duration (usually 2-3 months or more). However, it may be more meaningful to view CKD as a state marked by the permanent loss of functioning nephrons. This condition is irreversible, with no chance of complete recovery, although the remaining nephrons may undergo hypertrophy and hyperfiltration.
This blood test is a simple biochemical measure for assessing renal function. By evaluating the plasma concentrations of creatinine and urea, it allows for an estimation of the glomerular filtration rate (GFR), helping to determine if the kidneys are effectively filtering the blood.
Urine Specific Gravity(USG): The distinction between pre-renal and renal causes of azotemia is most often made on the basis of measurement of urine specific gravity (USG).
Glomerular Filtration Rate(GFR): The glomerular filtration rate (GFR) shows how well the kidneys are filtering. Obtaining an accurate GFR level is difficult because measured GFR (mGFR) involves a complex and time-consuming process, making it impractical for both clinicians and patients. As a result, healthcare professionals rely on a formula to estimate GFR. CKD often doesn’t present symptoms until its later stages, which is why having reliable GFR estimates is crucial for identifying the disease as early as possible.The standard way to estimate GFR is with a simple blood test that measures your creatinine levels.
Creatinine is a breakdown product of creatine phosphate in skeletal muscle, creatinine is produced at a constant daily rate. It is freely filtered by the kidneys, not reabsorbed, and is slowly secreted. The glomerular filtration rate (GFR) is inversely related to plasma creatinine concentration. Since creatinine levels are proportional to muscle mass, the result needs to be adjusted using the Modification of Diet in Renal Disease (MDRD) equation or equivalent GFR estimation equations to calculate the effective GFR (eGFR). Creatinine levels can also be influenced by factors such as pregnancy, muscle mass, and diet.Creatinine is less influenced by recent protein ingestion than urea.
Urea is a waste product formed from the breakdown of proteins. Urea is produced from ammonia derived from amino acids as part of the ornithine cycle within the liver. Amino acids used in the production of urea can originate either from endogenous or exogenous protein sources. Urea is filtered at the glomerulus but undergoes passive reabsorption within the tubules. The degree of reabsorption increases with slower tubular flow rates, which are typically identified in patients that are
either hypovolemic or dehydrated. The serum urea-to-creatinine ratio can help determine the origin of an acute kidney injury. While serum urea levels are commonly used to assess renal function, changes in urea levels can also indicate other underlying pathologies.
Proteinuria is the term used to describe the presence of increased amounts of protein within the urine.The glomerular filtration barrier, made up of the glomerular capillary endothelium, basement membrane, and epithelial podocytes, restricts the passage of medium and high molecular weight proteins from the blood into the glomerular filtrate, with albumin (69 kDa) and larger proteins typically being retained. In a healthy state, proteins that do filter through are efficiently reabsorbed by proximal tubular cells via megalin- and cubulin-mediated endocytosis, resulting in minimal proteinuria. Proteinuria can arise from structural or functional changes in the glomerular filtration barrier (glomerular proteinuria) or from a reduced ability of proximal tubular cells to reabsorb proteins (tubular proteinuria).
Hematuria refers to the presence of an excessive number of red blood cells (RBCs) in the urine, which can be either microscopic (detected only through dipstick or microscopic examination) or macroscopic (grossly visible). There are many potential causes of hematuria originating from the kidneys, but more commonly, it is linked to issues in the lower urinary tract (e.g., urinary tract infection) or systemic conditions (e.g., coagulopathy). It is important to differentiate these from hematuria caused by diseases in the genital tract.
Pyuria refers to the presence of increased white blood cells (WBC) in urine (Figure 321-5) and is most likely to
be identified in patients with urinary tract inflammation and infection.