Thread by @medrants

1/ #UncleBob opines for #5goodminutes on the labs from @CPSolvers Episode 95 @Sharminzi

Briefly - unfortunate woman in her 50s, severe brain injury, all input from IV & feeding tube, stage 4 decubitus ulcer, now has markedly increased urine output (3 l/day) & hypernatremia 159

2/ Has known CKD with previous creatinine of 2.5

Labs in hospital

161/4.0. 103/20. 50/2.5 98. (calcium not given)
Urine Na 46, K 9, Cl 49, osm 148
with ADH administration urine osms ~ 180

3/ The #VMR chat room knows that I seriously nerd out over these numbers. My thinking:

Hypernatremia is water-handling problem. The patient is not taking in as much free water as she is excreting. By definition hypernatremia is dehydration (not necessarily volume contraction).

4/ W/ hypernatremia we should have concentrated urine. Urine concentrates when ADH attaches to the principal cells and allows aquaporin-2 to allow free water to leave the tubule and enter the interstitium.

5/ Thus, this patient likely has a deficiency of ADH (DI) or something that interferes with ADH (nephrogenic DI). In adults, most nephrogenic DI occurs secondary to either lithium or hypercalcemia. We do not have a calcium level reported.

6/ Interpreting the urine osms:
Isosthenuria is the state in which the urine osms mirror the serum osms. Thus, this patient should have urine osms of at least (and likely greater than ~ 330 (rough estimate of serum osms). Why are the urine osms not maximally dilute?

7/ In order to maximally dilute the urine, we need the counter-current mechanism to be fully operational. With CKD (and I suspect this patient is at least stage 4 CKD) we "wash out" the gradient in the counter-current, making full concentration or dilution unreachable.

8/ Likely this patient cannot dilute to less than around 150.

The patient received DDAVP and did not concentrate the urine significantly more - excluding the problem of central DI. Patients with central DI have a dramatic response to DDAVP

9/ Thus we must assume the patient has nephrogenic DI - look for calcium (which is quickly reversible) or lithium (which is not always reversible). In this case, the patient had previously been taking lithium for bipolar disorder

10/ Comments on other labs

The patient has a huge anion gap - suspect that she had significant hyperphosphatemia - but she might have had some ketosis or mild lactic acidosis also.

11/ We cannot us the formulas to estimate her GFR. She likely has decreased muscle mass. This could explain her BUN/creat ratio. I suspect she has either stage 4 or 5 CKD. Would love to know her calcium and phosphate. Would note that she has significant anemia.

12/ Finally, why does a diuretic decrease free water output - particularly a thiazide? Hopefully you remember that thiazides work on the NaCl transporter. This site is also known as the diluting segment. Thiazides inhibit urinary dilution!

13/ This same segment also explains why thiazides can cause hyponatremia in some patients.

I hope these thoughts are somewhat helpful. Many learners have asked me to help them think through lab testing. Please let me know if this helps and if I should do more of this.