A 53-year-old woman is being treated for tuberculosis with INH and rifampin.
INH can result in impaired oxygen utilization, leading to lactic acidosis (type B), accumulation of lactate, and increased anion gap.
A 69-year-old woman is taking large amounts of aspirin for osteoarthritis, and now complains of ringing in her ears and nausea.
Chronic salicylate use can cause respiratory alkalosis. Severe salicylate toxicity results in an anion gap metabolic acidosis such as during an overdose. During acute hyperventilation, plasma bicarbonate concentrations fall by approximately 3 mEq/L when the arterial pressure of CO2 falls to about 25 mm Hg. Acute respiratory alkalosis can be caused by anxiety, central nervous system (CNS) disorders, drugs, or fever. Chronic respiratory alkalosis occurs in pregnancy and liver disease as well.
A 42-year-old man presents to hospital with dark black-colored stools and passing out while getting up. On examination he is diaphoretic, blood pressure 80/50 mm Hg supine, pulse 120/min, and the DRE is positive for melena. He is resuscitated in the emergency room. He has low urine output and develops renal failure from ATN. A few days later, his urine output increases to 200 cc/h
The diuretic phase of ATN is characterized by large losses of sodium and water.
A 27-year-old woman presents because she is feeling unwell. Her examination is normal, but her serum sodium is 115 mEq/L. Her urine lytes: sodium 55 mEq/L, osmolality 100 mOsm/L. This condition causes the greatest amount of medullary washout.
Primary polydipsia can cause greater medullary washout than either nephrogenic or central DI because primary polydipsia tends to cause expansion of the ECF volume. This tends to increase total delivery of sodium chloride and water to the inner medulla. It also increases renal blood flow, and increased flow through the vasa recta reduces ability to trap solutes in the medulla.
A 64-year-old man develops severe diarrhea after returning from a foreign holiday. He is hypovolemic clinically and is given normal saline. His serum sodium is 125 mEq/L and potassium is 2.5 mEq/L. He develops increased urine output with urine sodium of 10 mEq/L and osmolality of 200 mOsm/L. His polyuria can be caused by hypokalemia.
Nephrogenic DI can be caused by hypokalemia as well as hypercalcemia.
A 34-year-old man is brought for evaluation because of bizarre behavior. He comments that he is voiding all the time of clear water-like urine. He has a past history of schizophrenia for which he is taking a major tranquilizer.
Both thioridazine and chlorpromazine have been associated with primary polydipsia.
A 38-year-old man is admitted to hospital for investigation of polyuria and a low serum sodium concentration. After a fluid deprivation test, there was no change in his urine osmolality. He was then given vasopressin (DDAVP) with no change in urine volume or urine osmolality after 2 hours.
There is little or no response to vasopressin after fluid deprivation in complete nephrogenic DI. Incomplete nephrogenic DI will show some response.
A 67-year-old man is admitted to hospital after a stroke. He has swallowing difficulties, and a nasogastric feeding tube is inserted to provide high protein content nutrition. After starting the tube feeds, he develops large amounts of urine output. His serum sodium is normal, and the urine values are sodium 60 mEq/L and osmolality 420 mOsm/L.
High protein tube feeds may cause a solute diuresis because of excessive excretion of urea. Other causes of solute diuresis include glucosuria, mannitol, radiographic contrast media, and chronic renal failure
A 74-year-old man from a nursing home is not feeling well and is confused. He is not able to give any reliable history. His serum sodium is 120 mEq/L and osmolality is 265 mOsm/kg. On examination, his blood pressure is 100/50 mm Hg, pulse 100/min, and neck veins are not visible. His urine sodium is 40 mEq/L and urine osmolality is 330 mOsm/kg.
The combination of ECF volume contraction with high urinary sodium (20 mmol/L) suggests renal fluid loss. This is commonly caused by diuretics or glucosuria.
A 65-year-old woman is admitted to the hospital after a stroke resulting in left hemiparesis. She has no trouble swallowing and is on a full diet. One week later, on routine biochemistry, her sodium is 128 mEq/L and osmolality is 270 mOsm/kg. She has no symptoms and is euvolemic on clinical examination. Urine sodium is 40 mEq/L and urine osmolality is 450 mOsm/kg.
SIADH is associated with many CNS diseases including meningitis, encephalitis, tumors, trauma, stroke, and acute porphyria. It is assumed that antidiuretic hormone (ADH) in these patients is secreted in response to direct stimulation of the hypothalamic osmoreceptors.
A 42-year-old man is on amitriptyline for depression. Recently he has been feeling more lethargic and unwell. His clinical examination is normal. Serum sodium is 125 mEq/L and osmolality is 260 mOsm/kg, and urine sodium is 40 mEq/L and osmolality is 450 mOsm/kg.
Amitriptyline is one of the psychoactive drugs that cause SIADH. Others include phenothiazines, serotonin reuptake inhibitors, and monoamine oxidase inhibitors (MAOIs). Antineoplastic drugs such as vincristine and cyclophosphamide also cause SIADH, as does the hypoglycemic agent chlorpropamide.
A 32-year-old man is feeling unwell and brought to the hospital. His serum sodium is 125 mEq/L. On examination, his blood pressure is 110/70 mm Hg, pulse 110/min supine, and sitting up causes him to feel light-headed with a drop in his blood pressure. His urine sodium is 5 mEq/L and urine osmolality is 800 mOsm/kg.
The combination of ECF volume contraction and low urinary sodium (<10 mmol/L) suggests extrarenal sodium loss. Common causes are vomiting, diarrhea, or excessive sweating.
A 57-year-old man is referred for assessment of his low serum sodium of 125 mEq/L. On examination, he has pitting edema and elevated neck veins. His urine sodium is 10 mEq/L and urine osmolality 350 mOsm/kg.
Hyponatremia associated with nephrotic syndrome, cirrhosis, or CHF is characterized by edema. It is believed that the hyponatremia is caused by a decrease in “effective” circulating volume secondary to decreased cardiac output or sequestration of fluid.
A 63-year-old man is feeling unwell with symptoms of increased thirst and voiding. He is not taking any medications and there is no past medical history. Physical examination is normal, but his serum sodium is 130 mEq/L and serum osmolality is 310 mOsm/kg.
This man has osmotic diuresis and associated hyponatremia. The clue to the extra osmoles in the serum is the increased serum osmolality in the setting of hyponatremia. This situation is frequently seen in Type II diabetes.
A 30-year-old woman is having symptoms of muscle weakness and fatigue. On examination, her blood pressure is 120/80 mm Hg, pulse 80/min, JVP 4 cm, heart sounds normal, and lungs clear. Her serum potassium level is 2.5 mEq/L, and bicarbonate 30 mEq/L. The urine potassium is 10 mEq/L.
In patients who have prior diuretic use, resulting in hypokalemia at the time of evaluation, the bicarbonate tends to be elevated and the urine potassium low (<25 mmol/L).
A 55-year-old man is having symptoms of muscle weakness and fatigue. He has poorly controlled asthma and recently had an exacerbation. On examination, his blood pressure is 160/90 mm Hg, pulse 80/min, JVP 4 cm, heart sounds normal, and lungs clear. His serum potassium level is 2.5 mEq/L and bicarbonate 30 mEq/L. The urine potassium is 40 mEq/L. Plasma renin and aldosterone levels are low.
Glucocorticoid and licorice ingestion can result in hypertension with low plasma renin and aldosterone levels
A 44-year-old woman is having symptoms of muscle weakness and fatigue. On examination, her blood pressure is 120/80 mm Hg, pulse 80/min, JVP 4 cm, heart sounds normal, and lungs clear. Her serum potassium level is 2.5 mEq/L, bicarbonate 18 mEq/L, and anion gap is normal. The urine potassium is 40 mEq/L.
RTA types I and II cause hypokalemia with high potassium excretion (>25 mmol/L) and a low bicarbonate in the absence of hypertension. Diabetic ketoacidosis can also result in this constellation of findings
A 30-year-old man is having symtoms of muscle weakness, fatigue, and headaches. On examination, his blood pressure is 180/100 mm Hg, pulse 80/min, JVP 4 cm, heart sounds normal, and lungs clear. His serum potassium level is 2.5 mEq/L and bicarbonate 30 mEq/L. The urine potassium is 40 mEq/L. Plasma renin is low and aldosterone is high.
Primary hyperaldosteronism is characterized by hypertension with high plasma aldosterone and low plasma renin.
A 60-year-old woman is having symptoms of muscle weakness and fatigue. On examination, her blood pressure is 110/80 mm Hg, pulse 100/min, JVP 1 cm, heart sounds normal, and lungs clear. Her serum potassium level is 2.5 mEq/L, bicarbonate 15 mEq/L, and anion gap is normal. The urine potassium is 10 mEq/L.
In lower GI loss (diarrhea), the blood pressure is normal, the urine potassium is low (<25 mmol/L), and the bicarbonate is either normal or low.
A 14-year-old girl develops a rash, abdominal pain, and arthralgias. She is also experiencing some nausea, vomiting, and crampy abdominal pain. On examination, she has a palpable purpuric rash on her buttocks and lower legs, a tender abdomen, and no active joint inflammation. Her stools test positive for blood, and urinalysis reveals RBCs and RBC casts. Her renal function deteriorates rapidly over several days. A renal biopsy is performed.
Metabolic acidosis and respiratory alkalosis are seen in salicylate overdose.
A 47-year-old woman with RA is being treated with nonsteroidal anti-inflammatory drugs (NSAIDs) and gold. She develops acute shortness of breath with hypoxemia and is admitted to the hospital. Admission urinalysis reveals 4+ proteinuria but no active sediment. A renal biopsy is performed.
Gold is one of the drugs causing nephrotic syndrome secondary to membranous GN. Captopril and penicillamine have also been implicated. Signs and symptoms of nephrotic syndrome (low albumin, edema, hyperlipidemia) are common, and membranous GN is also associated with a thrombotic diathesis.
A 19-year-old man, who is otherwise healthy, is found to have RBCs in his urine. There is no proteinuria. Evaluation of his family reveals that his mother also has hematuria. She has minimal renal impairment and, other than being hard of hearing, is in good health. A renal biopsy might show.
This presentation is typical for an inherited disorder of basement membranes such as Alport’s syndrome. It is inherited as an X-linked dominant disorder. It is relatively benign in women but frequently progresses to ESRF in men. It is often associated with sensorineural hearing loss.
A 33-year-old man from Southeast Asia, without HIV infection, is diagnosed as having pulmonary tuberculosis. He is started on multiple medications, including INH and rifampin. Three months later, he has developed edema. Liver tests are normal, and serum creatinine is increased by 30% over baseline. Urinalysis reveals 4+ proteinuria. A renal biopsy is performed.
Rifampin can cause minimal change disease as well as more severe renal damage. The described case is typical for minimal change GN with nephrotic syndrome. Drug-induced minimal change GN frequently has an associated interstitial nephritis. INH is not usually associated with renal disease.
A 43-year-old man had a subarachnoid hemorrhage from an intracranial aneurysm 8 years ago. He has also had progressive renal impairment associated with hematuria. The most likely diagnosis is
The autosomal dominant form of polycystic kidney disease is often associated with hepatic cysts, intracranial aneurysms, and colonic diverticula. The occurrence of renal failure is usually in the third decade or later. Complications include infection, obstruction by stone or clot, and gross hematuria.
A 28-year-old man presents with a kidney stone. He is married to his first cousin, and 6 months earlier, his 8-year-old son had a kidney stone as well. The most likely diagnosis is
Many of the listed disorders can cause nephrolithiasis, but cystinuria is the most common cause of stones in childhood. It is a common inborn error of amino acid transport and is inherited as an autosomal recessive trait. The disorder affects transport of all dibasic amino acids (lysine, arginine, ornithine, and cystine) in the kidney and the gut, but symptoms arise from the overexcretion of cystine because it is the least soluble.
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