in preeclampsia and gestational hypertension due to decreased fractional excretion of calcium.
Here we report a case of a patient who presented with generalized weakness, persistent hypokalemia, hypocalciuria, hypomagnesemia, and hypochloremic alkalosis, all of which are consistent with the typical manifestations of GS.
Serum electrolyte analysis demonstrated persistent hypokalemia and hypomagnesemia, while his urine electrolyte analysis demonstrated persistent hypocalciuria. Blood gas analysis demonstrated persistent metabolic alkalosis.
 Renal tubular function is also affected leading to the manifestation of hypocalciuria
.  The 24-h urine protein excretion measurement has been the gold standard for diagnosis of preeclampsia, but it is an inconvenient and time-consuming test.
The laboratory tests result exhibited obviously low urine specific gravity, increased urine pH, hypokalemia, hypochloremia, hyperkaluria, hypocalciuria
, metabolic alkalosis, increased plasma renin activity and angiotensin II, and low blood pressure.
Key laboratory findings include hypokalemia, metabolic alkalosis, hypomagnesemia, and hypocalciuria
This might be responsible for hypocalciuria
Patients with suspected PHP should complete a 24-hour urine collection for calcium and creatinine clearance to distinguish PHP from benign familial hypercalcemic hypocalciuria
. The latter syndrome, which is uncommon, is suggested by a urinary calcium-to-creatinine clearance ratio of less than 0.01.
One female patient who exhibited mild hypercalcemia, low PTH (8.6 pg/mL), normal 25OHD, and hypocalciuria
was found to carry a de novo heterozygote mutation of the CaSR gene (p.994delK (C.2981del AGA) and was diagnosed as a case of familial hypocalciuric hypercalcemia (FHH).
Furthermore, although one of the typical features of FHH is hypocalciuria
, some patients may present with hypercalciuria caused by the distinct functions of the mutated CaSR in renal and parathyroid cells leading to the incorrect diagnosis of primary HPT (24).