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Initially diagnosis is typically established by creatine, creatinine, and guanidinoacetate measurement in the plasma, urine, and/or cerebrospinal fluid, as listed in the table below. [5] The levels of these biochemical markers can indicate which specific creatine disorder is present.
Individuals with AGAT deficiency are intellectually disabled and have muscle weakness. The symptoms of AGAT deficiency are caused by the lack of creatine in specific tissues, most notably muscle and brain. Oral creatine supplementation can be used to treat AGAT deficiency, with early intervention providing the best results.
This constellation of symptoms contrasts with the classical presentation of nephrotic syndrome (excessive proteinuria >3.5 g/day, low plasma albumin levels (hypoalbuminemia) <3 g/L, generalized edema, and hyperlipidemia). [8] [10] Signs and symptoms that are consistent with nephritic syndrome include: Hematuria (red blood cells in the urine) [11]
Symptoms can vary from person to person. Someone in early stage kidney disease may not feel sick or notice symptoms as they occur. When the kidneys fail to filter properly, waste accumulates in the blood and the body, a condition called azotemia. Very low levels of azotemia may produce few, if any, symptoms.
The GFR is derived from the serum creatinine and is proportional to 1/creatinine, i.e. it is a reciprocal relationship; the higher the creatinine, the lower the GFR. It reflects one aspect of kidney function, how efficiently the glomeruli – the filtering units – work. The normal GFR is 90–120 ml/min.
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The normal range of GFR, adjusted for body surface area, is 100–130 average 125 (mL/min)/(1.73 m 2) in men and 90–120 (mL/min)/(1.73 m 2) in women younger than the age of 40. In children, GFR measured by inulin clearance is 110 (mL/min)/(1.73 m 2 ) until 2 years of age in both sexes, and then it progressively decreases.