Renal disease diabetes insipidus

Vasopressin, also called antidiuretic hormone (ADH), exerts its action by affecting the permeability of the renal tubules to water. In the absence of vasopressin, less water is reabsorbed into the bloodstream, and a large volume of light yellow, dilute urine results. Patients with the rare disease diabetes insipidus do not produce vasopressin their urine is extremely voluminous and dilute. In the presence of vasopressin, the tubules become more permeable to water that is drawn into the capillaries, thus increasing blood volume. The reabsorption of water from the tubules produces a low volume of dark yellow, concentrated urine. (Diabetes insipidus is very different from diabetes mellitus, mentioned elsewhere in the text.)... 

Nephrotoxicity IDV potentially TDF Onset IDV—months after therapy TDF—weeks to months after therapy Symptoms IDV—asymptomatic rarely develop end-stage renal disease TDF—asymptomatic to symptoms of nephrogenic diabetes insipidus, Fanconi syndrome 1. History of renal disease 2. Concomitant use of nephrotoxic drugs Avoid use of other nephrotoxic drugs adequate hydration if on IDV monitor creatinine, urinalysis, serum potassium and phosphorus in patients at risk D/C offending agent, generally reversible supportive care electrolyte replacement as indicated... 

Nephrogenic diabetes insipidus (NDI) is characterized by renal tubular resistance to the antidiuretic effect of arginine vasopressin (AVP). NDI may be inherited as an autosomal dominant or X-linked recessive disorder. The autosomal dominant form of NDI results from mutations of the aquaporin 2 gene (AQP2). AQP2 encodes a water channel of the renal collecting duct. Its disruption causes autosomal dominant NDI (113,114) and occasionally recessive forms of the disease. 

Diabetes insipidus A disease marked by increased urination (polyuria) and excessive thirst (polydipsia) due to inadequate production of antidiuretic hormone (ADH) and/or a decrease in the renal response to ADH. 

Nephrogenic diabetes insipidus. This occurs when the kidney is unable to respond to antidiuretic hormone. Most commonly this is the result of renal disease, but mutations in the ADFl receptor gene or in the gene encoding aquaporin-2 have also been demonstrated in affected humans. 

Mellitus distinguishes this disease from diabetes insipidus, which is caused by impaired renal reabsorption of water. 

Nephrogenic Diabetes Insipidus. Failure of the kidney to respond to normal or increased concentrations of AVP can cause NDI. In the majority of these patients, AVP is mcapable of stimulating cychc adenosine monophosphate (cAMP) formation. Two causes have been described for this disorder (1) mutation in the vasopressin receptor and (2) mutations in the aquaporin-2 water channels. Hie vasopressin receptor mutation form of NDI is an X-chromosome-linked disorder that mostly affects males. Females are more likely to have the aquaporin-2 water channel gene defect on chromosome 12,ql2-13, which produces an autosomal recessive disease. Acquired forms of NDI may be caused by metabolic disorders (hypokalemia, hypercalcemia, and amyloidosis), drugs (hthium, demeclocycline, and barbiturates), and renal diseases (polycystic disease and chronic renal failure). NDI may also be seen in the absence of these factors (idiopathic). 

From Latin, meaning sweetened with honey." Refers to the presence of sugar in the urine of patients having the disease. Mellitus distinguishes this disease from diabetes insipidus, which is caused by impaired renal reabsorption of water. 

In this condition the renal tubules are unresponsive to antidiuretic hormone and, as such, the subject has polyuria. The condition may be congenital or acquired. Acquired nephrogenic diabetes insipidus can result from several causes, such as chronic renal disease, potassium deficiency including primary aldosteronism, drugs such as lithium, systemic diseases such as multiple myeloma, and chronic hypercalcemias, including hyperparathyroidism. The damage to the renal tubules... 

Renal Urine concentrating defect Chronic interstitial nephritis, nephrogenic diabetes insipidus, end stage renal disease[rare]... 

Renal Toxicity Tetracychnes may aggravate azotemia in patients with renal disease because of their catabolic effects. Doxycychne has fewer renal side effects than do other tetracychnes. Nephrogenic diabetes insipidus has been observed in some patients receiving demeclocychne, and this effect has been exploited to treat the syndrome of inappropriate secrehon of antidiurehc hormone (see Chapter 29). Fanconi syndrome has occurred in pahents taking outdated tetracychne, presumably due to toxic effects on the proximal tubule. 

Does the patient have any other conditions Heart disease, renal insufficiency, diabetes, or endocrine conditions (e.g., Cushing, hyperaldosteronism, diabetes insipidus, or SIADH), which could place the patient at high risk for fluid overload, dehydration, or electrolyte imbalance when combined with the current assault. 

Normal urine volume in an adult is about 800-2000 ml/day. Increases in urinary volume (polyuria) occur in conditions such as hysterical polydipsia, diabetes insipidus, diabetes mellitus and Addison s disease. Low urine output occurs in dehydration, oedema and certain renal disorders. 

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