The goal of this review is to present a comprehensive survey of the many intriguing facets of creatine (Cr) and creatinine metabolism, encompassing the pathways and regulation of Cr biosynthesis an...

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Creatine and Creatinine Metabolism

Metabolism of l-[guanidinooxy-14C]canavanine in the rat

To better understand the biosynthesis of guanidinosuccinic acid, we determined urea, arginine, and guanidinosuccinic acid levels in nondialyzed uremic and hyperargininemic patients. These substances were also determined during several years of therapy in one hyperargininemic patient. Interrelationships of guanidinosuccinic acid levels with their corresponding urea and arginine levels were assessed by linear correlation studies. In uremic patients, a significant positive linear correlation (r = .821, p < .001) was found between serum urea and guanidinosuccinic acid levels. A significant positive linear correlation was also found between serum urea levels and urinary guanidinosuccinic acid levels (r = .828, P < .001), but not between serum arginine levels and urinary guanidinosuccinic acid levels in hyperargininemic patients. In the intrahyperargininemic patient study, a similar significant positive correlation was found between serum urea levels and the corresponding urinary guanidinosuccinic acid levels (r = .866, P < .001); the correlation between serum arginine levels and the corresponding urinary guanidinosuccinic acid levels was smaller. The presented analytical findings in uremic and hyperargininemic patients clearly demonstrate a metabolic relationship between urea and guanidinosuccinic acid.

The pathobiochemistry of uremia and hyperargininemia further demonstrates a metabolic relationship between urea and guanidinosuccinic acid.

Arginine (Arg) produced from citrulline originates mostly from kidneys. Arg is involved in guanidino compound biosynthesis, which requires inter-organ co-operation. In renal insufficiency, citrulline accumulates in the plasma in proportion to renal damage. Thus, disturbances in Arg and guanidino compound metabolism are expected in several tissues. An original use of the model of nephrectomy based on ligating branches of the renal artery allowed us to investigate Arg and guanidino compound metabolism simultaneously in injured (left) and healthy (right) kidneys. The left kidney of adult rats was subjected to 72% nephrectomy. Non-operated, sham-operated and nephrectomized rats were studied for a period of 21 days. Constant renal growth was observed only in the healthy kidneys. Guanidino compound levels were modified transiently during the first 48 h. The metabolism and/or tissue content of several guanidino compounds were disturbed throughout the experimental period. Arg synthesis was greatly reduced in the injured kidney, while it increased in the healthy kidney. The renal production of guanidinoacetic acid decreased in the injured kidney and its urinary excretion was reduced. The experimentally proven toxins α-keto-δ-guanidinovaleric acid and guanidinosuccinic acid (GSA) accumulated only in the injured kidney. The urinary excretion of GSA and methylguanidine increased in nephrectomized rats.When the injured kidney grew again, the level of some guanidino compounds tended to normalize. Nephrectomy affected the guanidino compound levels and metabolism in muscles and liver. In conclusion, the specific accumulation of toxic guanidino compounds in the injured kidney reflects disturbances in renal metabolism and function. The healthy kidney compensates for the injured kidney's loss of metabolic functions (e.g. Arg: production). This model is excellent for investigating renal metabolism when a disease destroys a limited area in one kidney, as is observed in patients.

Influence of 72% injury in one kidney on several organs involved in guanidino compound metabolism: a time course study

Chromatography and electrophoresis of creatinine and other guanidino compounds.

In this automated system for assaying guanidino compounds, the compounds are resolved on an ion-exchange (Dowex 50) column, then reacted with phenanthrenequinone in alkaline solution. This mixture is then acidified and the resulting fluorescence is measured (lambda ex, 305 nm; lambda em, 395 nm). I applied the system to the analysis of urine from control rats and rats given L-canavanine, L-canavaninosuccinic acid, L-guanidinosuccinic acid, L-arginine, or urea, intraperitoneally. The recorder tracings are compared with those obtained for urine from healthy and uremic humans. After urea administration some guanidinosuccinate is excreted, along with substantial quantities of another substance that elutes just before guanidinosuccinate and so may be mistaken for it. Urine from uremic humans also shows this unidentified peak, but not urine from untreated rats or healthy humans. L-Canavanine gives rise, mainly, to guanidine and homoserine, apparently by reduction. Similarly, canavaninosuccinate is reduced to homoserine and guanidinosuccinate. Arginine gives rise to small quantities of guanidinosuccinate. Guanidinosuccinate is excreted mainly unchanged. When the guanidinosuccinate concentration is increased, excretion of guanidinoacetic acid is suppressed.

Metabolic relationship between urea and guanidino compounds as studied by automated fluorimetry of guanidino compounds in urine.

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Metabolic relationship between urea and guanidino compounds as studied by automated fluorimetry of guanidino compounds in urine.