ABSTRACT
Here we present a case of acute renal failure needing dialysis in a heroin addict patient chronically treated with Metadone. This give us the opportunity to review the renal effects of the main drugs of abuse, highlighting the shift occured from the four "old sisters" (Marijuana, Cocaine, Heroin and Amphetamine) to the news synthetic drugs (chiefly Synthetic Cathinones and Cannabinoids), that poses problems due to large diffusion, easy procurement, legal non-regulation and difficult analytical identification, raising medical and forensic questions. From a Nephrological point of view is essential to take great care over the need to diagnose this kind of pathology and to widen the search trying anyway to recognize the substances potentially involved.
Subject(s)
Acute Kidney Injury , Cocaine , Substance-Related Disorders , Heroin , Humans , Renal DialysisABSTRACT
The current emphasis on kinetics and in situ control of molecular exchanges, across the tubular membrane, has not been paralleled by corresponding improvements in our understanding of tubular behaviour at the macroscopic level of classical physiology. In this paper, we propose a mathematical rationalization of macroscopic tubular transport by means of a principal transport equation, originating from the law of mass action between substrate and carrier. The other equations, derived from the main one, demonstrate the possibility of distinguishing between transporters with low affinity and high capacity and transporters with high affinity and low capacity. Moreover, our model formalizes both tubular reabsorption and tubular secretion. Regarding the renal calcium handling, our model confirms the two-compartment system proposed by Mioni in 1971, with some important variants, which are in agreement with the fractional reabsorptions of this cation along the tubule, as verified by micro-puncture technique. To obtain the frequency distribution of saturated tubules, we have utilized the infinitesimal analysis method, starting from the equations proposed by Smith in 1943, concluding that all titration curves result from the combined effect of enzymatic approach and anatomical heterogeneity of the nephrons. The theoretical equations included in our manuscript reflect substantial and palpable physiological mechanisms able to suggest diagnosis and therapy of some electrolyte and hormonal disorders. At the end of this paper, we highlight advantages and disadvantages detectable by comparing our mathematical approach with Marshall's and Bijvoet's methods, proposed, respectively, in 1976 and 1984.
Subject(s)
Glycosuria/physiopathology , Kidney Tubules/metabolism , Renal Reabsorption/physiology , Water-Electrolyte Balance/physiology , Animals , Calcifediol/blood , Calcitriol/blood , Calcium/blood , Calcium/urine , Dogs , Glycosuria/blood , Glycosuria/urine , Humans , Kinetics , Mathematical Computing , Parathyroid Hormone/blood , Phenolsulfonphthalein/metabolism , Phosphates/blood , Phosphates/urineABSTRACT
The approach to acid-base chemistry in medicine includes several methods. Currently, the two most popular procedures are derived from Stewart's studies and from the bicarbonate/BE-based classical formulation. Another method, unfortunately little known, follows the Kildeberg theory applied to acid-base titration. By using the data produced by Dana Atchley in 1933, regarding electrolytes and blood gas analysis applied to diabetes, we compared the three aforementioned methods, in order to highlight their strengths and their weaknesses. The results obtained, by reprocessing the data of Atchley, have shown that Kildeberg's approach, unlike the other two methods, is consistent, rational and complete for describing the organ-physiological behavior of the hydrogen ion turnover in human organism. In contrast, the data obtained using the Stewart approach and the bicarbonate-based classical formulation are misleading and fail to specify which organs or systems are involved in causing or maintaining the diabetic acidosis. Stewart's approach, despite being considered 'quantitative', does not propose in any way the concept of 'an amount of acid' and becomes even more confusing, because it is not clear how to distinguish between 'strong' and 'weak' ions. As for Stewart's approach, the classical method makes no distinction between hydrogen ions managed by the intermediate metabolism and hydroxyl ions handled by the kidney, but, at least, it is based on the concept of titration (base-excess) and indirectly defines the concept of 'an amount of acid'. In conclusion, only Kildeberg's approach offers a complete understanding of the causes and remedies against any type of acid-base disturbance.