Disorders of Urinary Concentrating Ability
An impairment in the ability of the kidneys to concen-trate or dilute the urine appropriately can occur with one or more of the following abnormalities:
1. Inappropriate secretion of ADH. Either too muchor too little ADH secretion results in abnormal fluid handling by the kidneys.
2. Impairment of the countercurrent mechanism. Ahyperosmotic medullary interstitium is required for maximal urine concentrating ability. No matter how much ADH is present, maximal urine concentration is limited by the degree of hyperosmolarity of the medullary interstitium.
3. Inability of the distal tubule, collecting tubule, and collecting ducts to respond to ADH.
Failure to Produce ADH: “Central” Diabetes Insipidus. Aninability to produce or release ADH from the posterior pituitary can be caused by head injuries or infections, or it can be congenital. Because the distal tubular segments cannot reabsorb water in the absence of ADH, this con-dition, called “central” diabetes insipidus, results in the formation of a large volume of dilute urine, with urine volumes that can exceed 15 L/day. The thirst mecha-nisms, discussed later, are activated when excessive water is lost from the body; therefore, as long as the person drinks enough water, large decreases in body fluid water do not occur. The primary abnormal-ity observed clinically in people with this condition is the large volume of dilute urine. However, if water intake is restricted, as can occur in a hospital setting when fluid intake is restricted or the patient is uncon-scious (for example, because of a head injury), severe dehydration can rapidly occur.
The treatment for central diabetes insipidus is admin-istration of a synthetic analog of ADH, desmopressin, which acts selectively on V2 receptors to increase water permeability in the late distal and collecting tubules. Desmopressin can be given by injection, as a nasal spray, or orally, and rapidly restores urine output toward normal.
Inability of the Kidneys to Respond to ADH: “Nephrogenic” Diabetes Insipidus. There are circumstances in whichnormal or elevated levels of ADH are present but the renal tubular segments cannot respond appropriately. This condition is referred to as “nephrogenic” diabetesinsipidus because the abnormality resides in thekidneys. This abnormality can be due to either failure of the countercurrent mechanism to form a hyperosmotic renal medullary interstitium or failure of the distal and collecting tubules and collecting ducts to respond to ADH. In either case, large volumes of dilute urine are formed, which tends to cause dehydration unless fluid intake is increased by the same amount as urine volume is increased.
Many types of renal diseases can impair the concen-trating mechanism, especially those that damage the renal medulla. Also, impairment of the function of the loop of Henle, as occurs with diuretics that inhibit elec-trolyte reabsorption by this segment, can compromise urine concentrating ability. And certain drugs, such as lithium (used to treat manic-depressive disorders) and tetracyclines (used as antibiotics), can impair the ability of the distal nephron segments to respond to ADH.
Nephrogenic diabetes insipidus can be distinguished from central diabetes insipidus by administration of desmopressin, the synthetic analog of ADH. Lack of a prompt decrease in urine volume and an increase in urine osmolarity within 2 hours after injection of desmopressin is strongly suggestive of nephrogenic dia-betes insipidus. The treatment for nephrogenic diabetes insipidus is to correct, if possible, the underlying renal disorder. The hypernatremia can also be attenuated by a low-sodium diet and administration of a diuretic that enhances renal sodium excretion, such as a thiazide diuretic.
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