A 27-year-old alcoholic man presents with decreased appetite, mild generalized weakness, intermittent mild abdominal pain, perioral numbness, and some cramping ofhis hands and feet. His physical examination is initially normal. His laboratory returns with a sodium level of 140 mEq/L, potassium 4.0 mEq/L, calcium 6.9 mg/dL, albumin 3.5 g/dL, magnesium 0.7 mg/dL, and phosphorus 2.0 mg/dL. You go back to the patient and find that he has both a positive Trousseau and a positive Chvostek sign.
Which of the following is the most likely cause of the hypocalcemia?
One of the commonest causes of hypocalcemia is impaired parathormone (PTH) production. Hypomagnesemia causes decreased production of PTH as well as decreased end-organ response to the hormone. Alcohol causes increased urinary losses of magnesium which then leads to the mentioned effects on PTH and ultimately to hypocalcemia. While pancreatitis can cause hypocalcemia, this patient’s presentation does not suggest the condition. Osteoporosis and poor dietary intake do not lead to hypocalcemia unless the patient has vitamin D deficiency. Routine calcium levels are not accurate in the setting of a low albumin. To estimate the true calcium level, one may add 0.8 mg/dL to the observed calcium level for every 1 g reduction in the albumin level (from 4 used as normal). In this case, the albumin is not far from 4 and hence the calculation would change the low calcium level very little. An ionized calcium level is consistent and accurate regardless of the albumin level of a patient.
A 27-year-old woman presents to the emergency room with a panic attack. She appears healthy except for tachycardia and a respiratory rate of 30. Electrolytes include calcium 10.0 mg/dL, albumin 4.0 g/dL, phosphorus 0.8 mg/dL, and magnesium 1.5 mEq/L. Arterial blood gases include pH of 7.56, P CO2 21 mm Hg, and PO2 99 mm Hg.
Which of the following is the most likely cause of the hypophosphatemia?
Respiratory alkalosis is one of the commonest causes of hypophosphatemia; it results from shift of phosphate from the extracellular to the intracellular space. Hypomagnesemia alone would increase phosphorus by decreasing parathormone effect. Hyper-parathyroidism can decrease phosphorus, but not to this degree; also, calcium is not elevated. Severe hypophosphatemia is seen with malnutrition, especially during the refeeding stage when carbohydrate intake causes phosphate to shift into the intracellular space. Such patients have clear clinical evidence of malnutrition. In addition, malnutrition almost always causes hypoalbuminemia. Vitamin D deficiency is uncommon in this age group and would be associated with hypocalcemia.
A 50-year-old diabetic woman presents for follow-up of her hypertension. Her blood pressure is 152/96 in the office today and she brings in readings from home that are consistently in the same range over the past month. Her current medications are amlodipine 5 mg daily and hydro-chlorothiazide 25 mg daily. The diuretic was added when she developed peripheral edema on the amlodipine; now she has only trace peripheral edema. A spot urine specimen shows 280 µg of albumin per mg creatinine (microalbuminuria is present if this value is between 30 and 300 µg/mg).
What would be the best next therapeutic step in this patient?
By a variety of mechanisms, angiotensin-converting enzyme inhibitors and angiotensin receptor blockers help to preserve renal function in diabetes. Both classes of medication can cause hyperkalemia, so it is important to monitor serum potassium after initiation. A significant increase in serum creatinine may suggest the presence of renovascular hypertension. A common side effect of ACE inhibitors is a dry cough. A less frequent side effect would be angioedema. Clonidine has not been shown to slow the progression of diabetic renal disease, and often causes orthostatic hypotension, constipation, and erectile dysfunction. Although many diabetic patients receive beta-blockers because of coronary disease, these are not first-line drugs for preventing progression of renal failure. Because of low cost and proven efficacy, thiazide diuretics remain a good choice for the general population, but do not have a specific effect on the progression of renal disease. Short-acting dihydropyri-dine calcium-channel blockers (eg, nifedipine) may increase the incidence of stroke and myocardial infarction, and have no role in the treatment of hypertension.
A 29-year-old man with HIV, on a highly active antiretroviral therapy (HAART) regimen including the protease inhibitor indinavir, presents with severe edema and a serum creatinine of 2.0 mg/dL. He has had bone pain for 5 years and takes large amounts of acetaminophen with codeine, aspirin, and ibuprofen. He is on prophylactic trimethoprim-sulfamethoxazole. Blood pressure is 170/110; urinalysis shows 4+ protein, 5 to 10 RBC, 0 WBC; 24-hour urine protein is 6.2 g. The serum albumin is 1.9 g/L (normal above 3.7).
Which of the following is the most likely cause of his renal disease?
Although many glomerular lesions occur in association with HIV, focal glomerulosclerosis is by far the commonest etiology of this patient’s nephrotic syndrome. While focal sclerosis is more common in intravenous drug users with HIV, the lesion is different from so-called heroin nephropathy. Indinavir toxicity may cause tubular obstruction by crystals and is a cause of renal stones, but does not cause nephrotic syndrome. Analgesic nephropathy is a frequently unrecognized cause of occult renal failure. This entity requires at least 10 years of high-level analgesic use and may cause renal colic owing to papillary necrosis. Analgesic abuse nephropathy, however, is an interstitial disease and does not cause nephrotic range proteinuria. Trimethoprim-sulfamethoxazole may cause acute interstitial nephritis, but the patient does not have fever, rash, WBC casts, or eosinophils in the urinalysis. Again, interstitial diseases do not cause high-level proteinuria. Bilateral renal artery stenosis would be rare at this age and is associated with a normal urinalysis.
A 60-year-old man is brought in by ambulance and is unable to speak. The EMS personnel tell you that a neighbor informed them he has had a stroke in the past. There are no family members present. His serum sodium is 118 mEq/L.
Which of the following is the most helpful first step in the assessment of this patient’s hyponatremia?
The first step in the clinical assessment of hyponatremia is a thorough history and physical examination, including assessment of extracellular fluid status. Increased ECF in the setting of hyponatremia may be caused by heart failure, hepatic cirrhosis, nephrotic syndrome, or renal insufficiency. A normal ECF in the same setting would indicate a disorder such as SIADH, whereas a decreased ECF would prompt a search for the cause of the hypovolemia (GI or renal losses being the most common). In hypovolemic states, ADH release is stimulated by the decreased ECF volume status and leads to free-water retention. Remember that, even when ECF volume is decreased, hyponatremia almost always indicates free-water excess (hypotonicity).
Determination of plasma osmolality is helpful in the setting of hyponatremia to confirm the presence of hypotonicity. Most patients with hyponatremia will have a lowplasma osmolality. A high-plasma osmolality usually indicates hyperglycemia, and a normal-plasma osmolality can indicate “pseudohyponatremia” caused by disorders such as hyperproteinemia and hyperlipidemia. In this case, determination of ECF status from the physical examination (history would be limited owing to patient’s inability to communicate) would be the best first step. You would not wait for the plasma osmolality before beginning assessment and development of an initial differential diagnosis. Helpful laboratory assessment in the face of hyponatremia includes plasma osmolality, urine osmolality, and urine K and Na concentration. The plasma AVP assay is difficult to perform, and the result would not be available in time to help the patient. Proteinuria does not cause hyponatremia unless overt nephrotic syndrome is present. Chest xray and CT scan of the head are indicated if the patient is found to have SIADH (euvolemic hyponatremia), but SIADH cannot be diagnosed until the volume status is determined.
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