A 40-year-old previously healthy woman is found to have proteinuria. She has no personal or family history of kidney disease, hypertension, or diabetes mellitus. She had two normal pregnancies, and neither was accompanied by hypertension or proteinuria.
Her pulse rate is 74/min and blood pressure is 128/85 mm Hg. The rest of the physical examination is unremarkable.
Laboratory Studies
Serum creatinine 1.0 mg/dL
Blood urea nitrogen 15 mg/dL
Serum total protein 7.5 g/dL
Serum albumin 3.8 g/dL
Urinalysis 3+ protein, 1+ blood. Microscopic: 5-7 erythrocytes and 1-3 leukocytes per high-power field, granular and hyaline casts.
Urine protein 1.9g/24 h
One month later, the urine protein is 2.1g/24 h.
Which of the following tests is most likely to establish a diagnosis?
( A ) Kidney biopsy
( B ) Serum and urine protein electrophoresis
( C ) Renal ultrasound
( D ) Measurement of serum antinuclear antibody, C3, and C4
( E ) Measurement of antistreptolysin O
A thin 60-year-old woman is brought to the emergency room weak and lethargic. The temperature is 37.8 ºC (100 ºF), pulse rate 120/min, respiration rate 24/min, and blood pressure 80/50 mm Hg.
Laboratory Studies
Serum electrolytes
Sodium 114 meq/L
Potassium 6.5 meq/L
Chloride 88 meq/L
Bicarbonate 14 meq/L
Blood urea nitrogen 43 mg/dL
Serum creatinine 1.7 mg/dL
Plasma glucose 36 mg/dL
Urine sodium 45 meq/L
Urine osmolarity 280 mosm/kg H2O
Which of the following is the most likely diagnosis?
( A ) Syndrome of inappropriate antidiuretic hormone secretion (SIADH)
( B ) Distal type I renal tubular acidosis
( C ) Diarrhea
( D ) Adrenal insufficiency
( E ) Renal failure
A 45-year-old woman is discovered trapped beneath a concrete slab after an explosion. She is alert, but both legs are immobilized by debris. Rescue workers must work slowly to extricate the woman because the building is highly unstable. They predict that she will remain trapped for as long as 12 hours. She is alert and can drink.
In addition to keeping her warm, what else should be done?
( A ) Administer a β-blocker.
( B ) Start an intravenous infusion of saline solution at 500 mL/h.
( C ) Administer intravenous fluids at 500 ml/h after she is extricated.
( D ) Administer a calcium channel blocker.
( E ) Administer an endothelin antagonist
hi
b
d
b
cd45 ...hows studies goin you seem to have disappeared...
i agree with dr guest ....
hi dr guest!!
3b
Crush injury causes traumatic rhabdomyolysis, which results in disruption of the muscular metabolic functions and marked cellular swelling. The limb swelling can be so extensive as to compress the arterial supply within the limb and cause additional ischemic injury to the muscle. As a result of massive intracellular fluid accumulation, there is intravascular volume depletion. Intravascular volume contraction in combination with the release of nephrotoxic myoglobin precipitates acute renal failure.
Administration of massive amounts of intravenous fluid (often 8 to 12 L in the first 24 hours after crush injury) can limit or prevent acute renal failure. This should be instituted as soon as possible, in this case before the patient is extricated, because volume depletion occurs rapidly once the crushed limb is freed. The addition of bicarbonate or mannitol to intravenous fluids has also been advocated. Volume expansion will also assist renal potassium excretion. Hyperkalemia is an early, life-threatening complication of rhabdomyolysis. Administration of oral fluids only will not provide sufficient volume. Waiting to administer intravenous fluids until the patient arrives at the hospital results in a potentially detrimental delay. There is no clinical evidence to support the use of calcium channel blockers or any other pharmacologic agent. Studies in experimental animals suggest that iron chelators, oxygen radical scavengers, and endothelin antagonists might be of use, but they are not validated for clinical application
2d
This patient presents with hypotension, hypoglycemia, hyponatremia, hyperkalemia, and a normal“anion gap metabolic acidosis. Adrenal insufficiency is the only entity that can account for the constellation of abnormalities in this patient. Sodium losses from mineralocorticoid deficiency and intravascular volume depletion from glucocorticoid deficiency are the explanations for this patient™s hypotension and fever. Glucocorticoid deficiency explains her hypoglycemia. Nonosmotic stimulation of antidiuretic hormone (ADH) from decreased circulating volume and glucocorticoid deficiency as well as ADH-independent intrarenal factors result in free water retention and hyponatremia. Mineralocorticoid deficiency results in decreased renal excretion of potassium and hydrogen ions, producing hyperkalemia and a normal“anion gap metabolic acidosis. The urine sodium concentration of 45 meq/L in the setting of a decreased circulating volume is consistent with the renal sodium wasting seen with mineralocorticoid deficiency.
The syndrome of inappropriate antidiuretic hormone (SIADH) secretion can explain the hyponatremia, but it does not account for the other metabolic abnormalities. Distal renal tubular acidosis is associated with hypokalemia and normal“anion gap acidosis.
Diarrhea can cause hypovolemia, which in turn can cause a nonosmotic release of ADH, resulting in free water retention and hyponatremia. Bicarbonate losses in the stool will result in a normal“anion gap metabolic acidosis. However, hypokalemia, as opposed to hyperkalemia, will result as a consequence of stool potassium losses. In addition, a low urine sodium concentration (less then20 meq/L) would be expected in the setting of diarrhea-induced hypovolemia.
Renal failure can result in a hyponatremia, hyperkalemia, and a metabolic acidosis due to decreased free water, potassium, and hydrogen ion excretion; however, these abnormalities generally occur in patients with advanced renal failure. Hyperkalemic metabolic acidosis can be seen in patients with mild degrees of renal insufficiency secondary to tubulointerstitial disease or may be associated with hyporeninemic hypoaldosteronism; however, hyponatremia would not be expected unless the patient was drinking an excessive amount of water, and hypoglycemia would not be expected in that setting