Measuring serum creatinine is a useful and inexpensive method of evaluating renal dysfunction. Creatinine is a non-protein waste product of creatine phosphate metabolism by skeletal muscle tissue. Creatinine production is continuous and is proportional to muscle mass.
Creatinine is freely filtered and therefore the serum creatinine level depends on the Glomerular Filtration Rate (GFR). Renal dysfunction diminishes the ability to filter creatinine and the serum creatinine rises. If the serum creatinine level doubles, the GFR is considered to have been halved. A threefold increase is considered to reflect a 75% loss of kidney function.
Reference values for serum creatinine:
Increased serum creatinine levels are seen in:
Decreased creatinine levels may be seen in: the elderly, persons with small stature, decreased muscle mass, or inadequate dietary protein. Muscle atrophy can also result in decreased serum creatinine level. If muscle atrophy is suspected, assessment of serum creatine, an important enzyme necessary for normal muscle function, is done.
The only important pathological condition that causes a significant increase in the serum creatinine level is damage to a large number of nephrons. Unlike the BUN, the serum creatinine level is not affected by hepatic protein metabolism. Tests to measure serum creatinine, urine creatinine, and creatinine clearance are all used only to evaluate renal function. Only renal dysfunction changes the results. The serum creatinine level does not rise until at least half of the kidney's nephrons are destroyed or damaged. Because creatinine levels rise and fall more slowly than BUN levels, creatinine levels are often preferred to monitor renal function on a long-term basis.
Serum creatinine and Blood Urea nitrogen (BUN) are often compared to evaluate renal function. While serum creatinine increases only with nephron damage, the BUN is affected by hydration, hepatic metabolism of protein and reduced GFR. The mean ratio of serum creatinine to the BUN should be approximately 1:10.
|NEPHROTOXIC DRUG||REDUCE TOXICITY|
The kidney's properties of high blood flow, filtration, reabsorption and concentration allow nephrotoxins to accumulate. A patient's BUN and creatinine should always be checked before giving nephrotoxic drugs. If either level is above the normal range, the drug should be held and the patient's physician should be contacted.
The commonly prescribed aminoglycoside antibiotics have both potential nephrotoxic and ototoxic effects. The impaired hearing or dizziness that may result from ototoxity is more likely if the drug is continued when there is renal dysfunction. It is also important to keep the patient well hydrated when aminoglycoside antibiotics are given because they are excreted almost unchanged in the urine.