Inferring ADH Defect from Urine Osmolality?

[pone]

I am trying to understand the interaction between urine osmolality, serum osmolality, and ADH regulation by the hypothalamus.

Assume a urine osmolality of 170 mOsmol/kg after 12 hours of water restriction. Proper value should be greater than 850. Low urine osmolality means highly dilute urine. In such a case, would you expect the serum osmolality to go very high due to inappropriately high urination under conditions of dehydration? Would the (potential) ADH defect here be a failure to create sufficient ADH in face of high serum osmolality?

What metabolites here would confirm whether the defect is in ADH response or in kidney response to proper ADH release?

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[Jabbed]

Assuming that you start with hypernatremia..

Polyuria of >3L per 24 hr period suggests osmotic diuresis or diabetes insipidus. Urine osmolality > 300 mOsm/L suggests osmotic diuresis (glucose, urea, saline). Urine osmolality < 150 mOsm/L suggests diabetes insipidus d/t ADH failure. Differentiation between central diabetes insipidus and nephrogenic is made either by history or empirically by administering desmopressin (continued dilute urine suggests nephrogenic cause, corrected urine osmolality suggests central etiology).

 

[Mr. Mojo Risin]

If you're suspecting DI, a desmopressin stimulation test could differentiate between central and nephrogenic. If it's central, then stimulation will replace the deficiency. If it's nephrogenic, stimulation isn't going to do anything.

 

[pone]

Assuming that you start with hypernatremia..

Polyuria of >3L per 24 hr period suggests osmotic diuresis or diabetes insipidus. Urine osmolality > 300 mOsm/L suggests osmotic diuresis (glucose, urea, saline). Urine osmolality < 150 mOsm/L suggests diabetes insipidus d/t ADH failure. Differentiation between central diabetes insipidus and nephrogenic is made either by history or empirically by administering desmopressin (continued dilute urine suggests nephrogenic cause, corrected urine osmolality suggests central etiology).

Jabbed I followed this except for the hypernatremia. What if you are starting from a serum sodium value in the normal range?

Thanks for the insights on desmopressin.

 

[Jabbed]

Jabbed I followed this except for the hypernatremia. What if you are starting from a serum sodium value in the normal range?

Thanks for the insights on desmopressin.

Remember that serum sodium evaluates water balance.
If your serum sodium is normal then your free water level is balanced. There is either no ADH defect, or you have corrected for it through hypotonic fluid therapy.

 

[pone]

Remember that serum sodium evaluates water balance.
If your serum sodium is normal then your free water level is balanced. There is either no ADH defect, or you have corrected for it through hypotonic fluid therapy.

So if patient has:

* polyuria of more than 3 litres per 24 hr period
* urine osmolality < 150 mOsmol/kg after 12 hours of water restriction
* reports abnormal level of thirst
* normal serum sodium

this would not be considered pathological? How might we characterize such an individual? Such a person simply has an inability to store water but the brain and kidneys are managing the electrolytes appropriately?

 

[Jabbed]

So if patient has:

* polyuria of more than 3 litres per 24 hr period
* urine osmolality < 150 mOsmol/kg after 12 hours of water restriction
* reports abnormal level of thirst
* normal serum sodium

this would not be considered pathological? How might we characterize such an individual? Such a person simply has an inability to store water but the brain and kidneys are managing the electrolytes appropriately?

I would not think that to be physiologically possible. Is there a particular qbank question that you're referencing?

 

[pone]

I would not think that to be physiologically possible. Is there a particular qbank question that you're referencing?

I have access to the data for an unpublished study on chronic fatigue, and I'm noticing a pattern where many of the inputs follow that pattern. The actual urine osmolality numbers are typically >150 and <200, but still low when they should be >800 after fluid restriction. It seems quite weird, and I was just wondering if such a condition suggested anything. I guess it is not a disease but I was struggling to understand what it suggests about the underlying physiology.

 

[Jabbed]

I have access to the data for an unpublished study on chronic fatigue, and I'm noticing a pattern where many of the inputs follow that pattern. The actual urine osmolality numbers are typically >150 and <200, but still low when they should be >800 after fluid restriction. It seems quite weird, and I was just wondering if such a condition suggested anything. I guess it is not a disease but I was struggling to understand what it suggests about the underlying physiology.

Your chronic fatigue patients are on lasix.

Without fluids restriction, decreased activity of the thick ascending limb leads to isosmotic fluid loss, so serum sodium is normal. BUT, the combination of fluid restriction after washing out their corticopapillary gradient leads to an inability to concentrate urine and gives you the illusion of "mild" nephrogenic diabetes insipidus.

 

[pone]

Your chronic fatigue patients are on lasix.

Without fluids restriction, decreased activity of the thick ascending limb leads to isosmotic fluid loss, so serum sodium is normal. BUT, the combination of fluid restriction after washing out their corticopapillary gradient leads to an inability to concentrate urine and gives you the illusion of "mild" nephrogenic diabetes insipidus.

Would that mechanism of action be unique to Furosemide/Lasix, or would any diuretic behave in a similar way? I'm not seeing Lasix listed for any of the specific records I am looking at, but now you have me wondering could it just be a diuretic in the diet? It's hard to believe that anyone could be drinking that much caffeinated beverage, for example. Maybe they take some weight loss supplement or other over-the-counter that acts like a diuretic?