A 65-year-old male admitted to the ICU with septic shock and develops nonoliguric AKI. Urinary microscopy reveals muddy brown, granular, and epithelial cell casts. Serum creatinine does not improve with fluid resuscitation. Which of the following sets of laboratory parameters is MOST consistent with a diagnosis of acute tubular necrosis?
FENa fractional excretion of sodium; Scr, serum creatinine.
Correct Answer: D
There are three major diagnostic approaches that are used to distinguish prerenal disease from ATN:
References:
A 42-year-old female presents with acute oliguric renal failure 3 days after initiation of chemotherapy for newly diagnosed non-Hodgkin lymphoma. Urine sediment analysis demonstrates amber crystals shaped like hexagonal plates, barrels, and needles.
Which of the following therapies is LEAST likely to be beneficial in the prophylaxis and management of this nephropathy?
This patient most likely has tumor lysis syndrome (TLS) and AKI as a consequence. Uric acid precipitation in the renal tubules results in AKI in patients with acute urate nephropathy. This could occur due to overproduction and excretion of the excess uric acid, particularly after chemotherapy or radiation in patients with lymphoma, leukemia, or other myeloproliferative diseases. That being said, patients with a large tumor burden could present with spontaneous TLS, without antecedent chemotherapy.
Uric acid nephrolithiasis may manifest with flank pain if there is renal pelvic or ureteral obstruction. The diagnosis should be suspected in presence of acute renal failure in patients at high risk for TLS (increased tumor burden, volume depletion, preexisting CKD, and hyperuricemia). Uric acid nephropathy is associated with a marked hyperuricemia, with plasma urate levels >15 mg/dL. Urinalysis may show uric acid crystals.
Prophylaxis in patients at high risk for TLS involves the use of allopurinol or febuxostat (xanthine oxidase inhibitors) along with rasburicase (recombinant urase oxidase that catalyzes conversion of uric acid to allantoin). The cornerstone of treatment of TLS and urate nephropathy is aggressive intravenous hydration to ensure adequate renal blood flow and glomerular filtration. Volume expansion has shown to delay and reduce the need for renal replacement therapy in these patients. Sodium bicarbonate infusion and alkalization of urine could reduce solubility and increase the risk of calcium phosphate precipitation. Further rise in serum pH with bicarbonate infusion could result in exacerbation in hypocalcemia. For these reasons, urinary alkalinization is not recommended in this setting.
A 33-year-old male underwent a necrosectomy for necrotizing pancreatitis 4 days ago. For the past 2 days, he has been complaining of watery diarrhea. He has not noticed any blood in his stool. Laboratory parameters are as follows:
Which of the following findings in this patient would be MOST consistent with metabolic acidosis attributed to diarrhea?
Correct Answer: B
This patient has hyperchloremic, nonanion gap metabolic acidosis due to excessive GI bicarbonate loss consequent to diarrhea. The response of the kidneys in this case is to reabsorb the chloride instead of bicarbonate, yielding no net change in the serum anion gap (AG).
Measurement of serum anion gap helps deduce the etiology for metabolic acidosis. Serum AG represents the difference in the measured cations (mainly sodium) and anions (chloride and bicarbonate). Serum AG is usually around 12 ± 4 mEq/L but can vary depending on the laboratory. Hyperchloremic metabolic acidosis could result from impaired renal acid excretion, bicarbonate loss, or administration of chloride-rich solutions during resuscitation.
UAG is the difference between measured urine cations and anions (UAG = Na + K − Cl) and helps differentiate renal causes of non–anion gap acidosis from the gastrointestinal causes.
Normally, the sum of the excreted urine sodium and urine potassium is greater than the amount of excreted urine chloride resulting in a positive UAG. With diarrhea and other nonrenal causes of hyperchloremic acidosis, the kidneys compensate by increasing the net acid excretion. The excretion of ammonium occurs in conjunction with chloride. In such situations, urine chloride exceeds the sum of urine sodium and potassium, resulting in a negative UAG. Urine AG is a useful tool to differentiate renal from GI causes in hyperchloremic metabolic acidosis.
A 38-year-old male with multiple enterocutaneous fistulae and chronic malnutrition on total parenteral nutrition (TPN) is admitted to the ICU with lethargy and hypotension. His medical history is significant for Crohn disease requiring multiple bowel surgeries. Soon after arrival in the ICU, he starts seizing and exhibits tetany.
Which of the following electrolyte abnormalities is MOST consistent with this presentation?
Hypomagnesemia is a common in critically ill patients. Magnesium plays an important role in several vital biochemical and physiological functions of the body including neuromuscular and cardiac conduction, maintenance of cardiac contractility, and vascular tone.
Hypomagnesemia could result from either gastrointestinal (GI) or renal losses. GI causes include diarrhea, intestinal fistulae, and malabsorption syndromes. Renal causes include chronic parenteral fluid therapy, osmotic diuretics, and chronic alcohol consumption. It is important to note that several medications including diuretics, antibiotics, and immunosuppressants can lead to hypomagnesemia through renal mechanisms.
Intracellular magnesium depletion has potential to cause atrial and ventricular arrhythmias, impaired cardiac contractility, and vasoconstriction. Nervous system manifestations include hyperactivity, tremors, and tetany with a positive chvostek sign. Severe hypomagnesemia could result in altered mental status and seizures. Magnesium depletion can present with neuromuscular symptoms that are similar to those of calcium deficiency, including hyperactive reflexes, muscle tremors, and tetany.
A 19-year-old female was on a hiking trip with her friends who brought her to the emergency room with lethargy. The only significant medical history she mentions is that she has diabetes and problems with her thyroid. Other than hypotension, the rest of her physical examination is unrevealing.
Which of the following clinical profiles is MOST consistent with a diagnosis of adrenal insufficiency in this patient?
Correct Answer: C
Patients with type 2 polyendocrine syndrome could present with type 1 diabetes, thyroid autoimmunity, and adrenal insufficiency. Hyponatremia and hyperkalemia are commonly seen in patients with adrenal insufficiency due to diminished cortisol and aldosterone production.
Aldosterone enhances sodium reabsorption and increases urinary potassium secretion. The hyperkalemia that is seen in adrenal insufficiency is largely related to the aldosterone deficiency. Cortisol has a direct suppressive effect on antidiuretic hormone (ADH) secretion, and a deficiency of cortisol results in hyponatremia due to the effect of increased ADH.
Treatment of hyponatremia in adrenal insufficiency requires cortisol and volume repletion. The administration of saline alone is relatively ineffective as the water retention due to ADH persists if cortisol is not supplemented. Cortisol replacement with hydrocortisone helps with the potassium excretion through its mineralocorticoid activity. Hypoaldosteronism should be considered in patients with persistent hyperkalemia accompanied by hyponatremia.
References :
Click to expand