Consult rounds: Electrolyte abnormalities associated with Primary hyperparathyroidism

Classically, we are notified to see a patient with hypercalcemia and one of the diagnosis that is made is primary hyperparathyroidism (PHPT). Due to the elevated PTH, what other electrolytes can go out of order?

1.       Hypophosphatemia:  Elevated PTH levels tend to lead to phosphate wasting in the urine.  Proximal tubular absorption of phosphorus( Na –Phos co transporter)  is blocked leading to renal wasting.

2.       Hypomagnesemia: This one is interesting as hypercalcemia would lead to decrease magnesium absorption via Ca-Sensing receptor in the TAL but PTH would increase magnesium absorption.  But net effect usually is “ hypercalcemia” wins leading to mg wasting as well. This in turn might lead to hypokalemia as well.

3.       Metabolic acidosis: Elevated PTH levels lead to decrease proximal bicarbonate absorption and leading to mild metabolic acidosis. This is usually seen when you have AKI as well compounding this problem.

   

Topic Discussion: Glomerular Diseases and Pregnancy

Many times, primary GN presents during pregnancy and diagnosis is tough. Other times, patients with known primary GN get pregnant.  Three questions come to mind.

1.       Does the pregnancy change the natural course of the glomerular disease?

A study done in over 120 pregnancies looked at this question. The clinical course of 123 pregnancies in 86 patients with biopsy-proven glomerular diseases was evaluated. No complications were observed in more than half of the pregnancies. The lowest incidence of complications was observed in patients with membranous nephropathy and the highest in membranoproliferative glomerulonephritis(MPGN) patients. Renal function deteriorated in 10 cases during pregnancy. The authors note that in most patients pregnancy did not change the natural history of glomerular disease.

2.       What are the risk factors in GN with pregnancy for maternal and fetal outcomes?

Hypertension and impaired renal function at conception seem to carry increased risk for mothers and fetuses. A study done at a single center looked at these complications. 24 pregnancies in 17 women with biopsy-proven glomerular disease was analyzed. The underlying renal histology was IgA nephropathy in 8 cases, lupus nephritis in 7, MPGN in 1, and focal segmental glomerulosclerosis in 1.

                Fetal survival rate was 75%. The perinatal mortality was 5.5%. De novo hypertension occurred in 8 pregnancies (33.3%). In 11 pregnancies (46%) increased proteinuria was diagnosed and in 6 (25%) a decline in maternal renal function was recorded. Maternal hypertension and renal function impairment were found to lead to more ob complications.  

3. Which GN fare the worse?

Many GN have been reported with pregnancy( Membranous GN, MCD, MPGN, IgA, FSGS). A single center study looked at outcomes based on type of GN in pregnancy. In all cases diagnoses were established by biopsy before pregnancy. They were: MPGN in 16 patients, focal glomeruloesclerosis in 13, IgA nephropathy in 10, membranous nephropathy in seven and focal glomerulonephritis in two women. Women with membranoproliferative glomerulonephritis appeared to fare worse, and those with IgA nephropathy and membranous nephropathy better than the rest.

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Pseudohyperkalemia: Some questions and possible answers?

Pseudohyperkalemia- what’s the mechanism and why?

Classically, we observe this in patients who have thrombocytosis or leukocytosis. Potassium is released from WBCS and platelets when a blood sample is allowed to clot in vitro.   When we use a plasma sample, the tube it gets drawn is heparinized and hence clotting doesn’t occur and plasma K levels are usually lower than serum K levels. When you have thrombocytosis or leukocytosis, this process is even more prominent.   In thrombocytosis, platelet granules release K.

Besides the clotting leading to lysis and K release, prolonged storage of blood at room temperature or in cold before performing the test and lead to impair N/K ATPase pump in WBCS and lead to spurious K levels.

Some researchers have defined pseudohyperkalemia when serum potassium concentration exceeded that of plasma by more than 0.4 mmol/L provided that samples are collected under strict techniques, remain at room temperature and are tested within 1 hour from blood specimen collection.

The phenomenon of pseudohyperkalemia was first reported by Hartmann and Mellinkoff in 1955 as a marked elevation of serum potassium levels in the absence of clinical evidence of electrolyte imbalance. They also found that in particular, the lag time between blood collection and potassium determination was confined to a maximum of 30 minutes, and a positive correlation between platelet count and serum, but not plasma potassium concentration, was found. Other causes of this entity is from fist clenching and use of tourniquet as well.

With leukemia, many cases are now reported leading to false elevation of K.  If plasma and serum are separated quickly ( within 30 min), the normal K levels can be seen.  Potassium normally is now measured in heparinized tubes, so why does K still get elevated?  Lysis of cells can still occur.  Because of the high WBCS counts seen in some cases of CLL, spurious K can still be found. It is possible that its due to the impaired N/K pump in that state of elevated WBCs that contribute to the release of K from cells.  Trauma is the major cause. Drawing in a tube without shaking may help as well.

What about Stat ABG draws? The fragile WBCs are prone to mechanical stress frequently. The K measurements in many cases of CLL may be inaccurately elevated if sample of blood are not analyzed quickly and in absence of lysis inducing events. Arterial analysis done by ABG draws is quicker and perhaps less mechanical stress and may allow for more accurate K readings than venous draws.  In addition, perhaps it also doesn’t allow for that fist clenching and tourniquet use that might be leading to pseudohyperkelamia.

Is plasma K better than serum K?  A letter in NEJM in 1991 showed that elegantly that plasma K was superior to serum K in getting the more accurate K level in patients who had experienced trauma.

What is reverse pseudohyperkalemia? It is when the plasma K is higher than serum K and still is spurious in nature. Few cases reports have highlighted this entity as well. It is possible that this is due to a hiegtened sensitivity to heparin induced membrane damage in setting of a blood malignancy.