First Aid: Renal Flashcards
A neonate presents with limb deformities, facial anomalies (low set ears and retroganthia), chest compression and pulmonary hypoplasia. What is this fetus suffering from and what are some possible causes?
POTTER Syndrome Pulmonary hypoplasia Oligohydramnios (trigger) Twisted face Twisted Skin Extremity Defects Renal Failure (in utero)
Causes: ARPKD, posterior urethral valves, bilateral renal agenesis
What are patients with Horseshoe kidney at increased risk of developing? What major syndrome is this condition associated with?
- Increased risk for ureteropelvic junction obstruction
- hydronephrosis
- renal stones
- rarely renal cancer (Wilms Tumor)
Associated with Turner syndrome
Abnormal interaction between ureteric bud and metanephric mesenchyme (which leads to glomerular development) results in what condition?
Multi cystic dysplastic kidney - nonfunctioning kidneys with cysts and connective tissue
Asymptomatic if unilateral, with compensatory Hypertrophy of opposite kidney
What is a main concern in a procedure like hysterectomy?
Ligation of uterine vessels may damage the ureter leading to ureteral obstruction or leak.
“Water under the bridge”
In which condition is the charge barrier lost for glomerular filtration? What results?
Nephrotic Syndrome
Albuminuria, hypoproteinemia, generalized edema, hyperlipidemia
Where do NSAIDs exert their effects on the glomerulus? What about ACE inhibitors?
Normally prostaglandins dilate afferent arterioles, so NSAID will block here and cause constriction.
Normally Angiotensin II constricts efferent arterioles, so ACE INHIBITORS will block here causing dilation.
A patient is administered an NSAID, what would happen to the filtration fraction? What about if ACE inhibitors were given?
FF = GFR / RPF
NSAID –> constriction of afferent arteriole (normally prostaglandins would dilate) –> decrease RPF and GFR –> FF remains constant
ACEI –> dilation of efferent arteriole (normally angiotensin II would constrict) –> increase RPF and decrease GFR –> FF decreases
Think the opposite without the presence of drug
A pregnant woman gives a urine sample. What would you expect of glucose and amino acid levels?
During pregnancy it is normal to have decreased reabsorption of glucose and amino acids at proximal tubule, so you would see glucosuria and aminoaciduria.
Plasma glucose of 200 mg/dL is threshold for glucosuria to begin, at 375 mg/dL all transporters in proximal tubule become saturated
A patient presents with neutral aminoaciduria and decreased absorption of these amino acids in the gut. They have pellagra like symptoms. What should you treat them with?
Hartnup Disease - autosomal recessive disorder - decreased reabsorption of neutral amino acids in renal tubular cells and enterocytes.
Treat with high protein diet and nicotinic acid
What two things will increase water reabsorption in the collecting tubules? What two things will decrease water reabsorption here?
Aldosterone increases Na channel insertion on lumen –> increased Na absorption –> increased H2O absorption
ADH Mobilized aquaporins, increasing H2O reabsorption
Potassium sparing diuretics will counteract and increase H2O excretion: the K+ STAys –> Spironolactone (aldosterone receptor antagonist), Triamtrene, Amiloride (blocks Na channels)
Name all of the renal tubular defects, the resultant dysfunction and if applicable, their causes.
“The kidneys put out FABulous Glittering Liquid.”
FAnconi syndrome (PCT): increased excretion of all amino acids, glucose, bicarb, and phosphate. Hereditary defects (Wilson Disease), ischemia, nephrotoxins/drugs.
Bartter Syndrome (thick ascending loop): AR affecting Na/K/2Cl cotransporter. Hypokalemia and metabolic alkalosis w/ hypercalcuria.
Gitelman Syndrome (DCT): AR, reabsorptive defect of NaCl. Hypokalemia and metabolic alkalosis, NO hypercalcuria.
Liddle Syndrome (collecting ducts): AD, increased Na reabsorption. HTN, hypokalemia, metabolic alkalosis, decreased aldosterone.
What factors will induce the kidneys to secrete renin? What is responsible for secreting renin?
- decreased BP (JG cells)
- decreased Na delivery (macula densa cells)
- increased sympathetic tone (beta-1 receptors)
- Tumors - paraneoplastic syndrome
Juxtaglomerular apparatus
What are the major affects of Angiotensin II on the body? What occurs on the organ level to allow for this?
Helps maintain blood volume and blood pressure, while limiting reflex bradycardia.
Increased reabsorption of Water and Salt, increased excretion of K+ and H+.
Overall vasoconstriction. Preferential constriction of efferent arteriole.
What compound acts as a “check” on the renin-angiotensin -aldosterone system? What results from its action?
Atrial Natriuretic Peptide (ANP) - which relaxes vascular smooth muscle via cGMP causing increased GFR and decreased renin.
There is also increased Na filtration without compensatory increased reabsorption. Net Na and volume loss.
From where is erythropoietin released?
Interstitial cells in the peritubular capillary beds (in response to hypoxia).
What induces the release of ADH? What about PTH?
What is the result of their action?
ADH - increased plasma osmolarity, decreased blood volume. Causes increased H2O reabsorption.
PTH - decreased Ca, increased Phsophate, decreased vitamin D. Causes increased Ca reabsorption (DCT), decreased phosphate reabsorption (PCT) and increased Vit D production
What are the possible factors for inducing hyperkalemia in patients?
DO Insulin LAB work. INsulin shifts K+ INto cells.
Digitalis hyper-Osmolarity INSULIN deficiency Lysis of cells Acidosis Beta-adrenergic antagonist
A patient presents with low pH and low pCO2. They are hyperventilating. What do you want to check next and how?
Metabolic acidosis with compensation –> Check ANION GAP
Anion Gap = Na+ - (Cl- + HCO3-)
A patient presents with flank tenderness, hematuria, colicky pain radiating to groin, and abdominal pain. They seem to be very anxious and are confused. What ion may there be a high serum concentration of?
Calcium
Stones (renal), bones (pain), groans (abdominal pain), psychiatric overtones (anxiety, altered mental status).
Will not necessarily have calciuria.
A hyperventilating patient with metabolic acidosis has a high anion gap (»12 mEq/L). What are the possibilities for this condition? What if the anion gap was normal (8-12 mEq/L)?
High anion gap = MUDPILES Methanol (formic acid) Uremia Diabetic Ketoacidosis Propylene glycol Iron tablets or INH Lactic Acidosis Ethylene glycol (oxalic acid) Salicylates (late)
Normal anion gap = HARD ASS Hyperalimentation Addison Disease Renal tubular acidosis Diarrhea Acetazolamide Spironolactone Saline infusion
A patient presents with massive proteinuria (>3.5g/day, frothy urine), hyperlipidemia, edema, and fatty casts in the urine. What other problems may this person’s disorder be associated with and why?
NephrOtic Syndrome
Hypoalbuminemia and Hyperlipidemia already mentioned also can have,
- Hypercoaguable state - Thromboembolism (due to ATIII loss in urine)
- Hypogammaglobulinemia - increased risk of infection (loss of immunoglobulins)
A young AA woman who is HIV+ presents with massive proteinuria, edema and fatty casts in urine. They have a fever and show signs of infection. A kidney biopsy is taken. What would you see on histology, IF and EM? What are the other associations for this person’s disorder?
Focal Segmental Glomerulosclerosis (NOS) - inconsistent response to steroid therapy
Histo: Segmental sclerosis of a glomerulus and hyalinosis (pink staining)
IF negative
EM: Effacement of foot process
Most common NOS in AAs and Hispanics. Associated with HIV infection, sickle cell, heroin abuse, massive obesity, interferon treatment, and chronic kidney disease due to congenital absence or surgical removal.
A middle aged white man presents with massive proteinuria, fatty casts in urine and edema. He was otherwise in normal health, had no major disease or infections in the past, and was not taking any drugs. A kidney biopsy is taken and reveals diffuse capillary and glomerular basement membrane thickening on light microscopy. What would IF and EM reveal? What are the common associations for his condition?
Membranous Nephropathy - poor response to steroid therapy
IF - positive, granular, from immune complex deposition
EM - “spike and dome” appearance with subepithelial deposits of the immune complexes
Associated with antibody phospholipase A2 receptor, drugs (NSAIDs & penicillamine), infections (HBV, HCV), Lupus, solid tumors.
A young girl presents with symptoms consistent with Nephrotic Syndrome. Her mother states that she recently had a bad case of the cold. A biopsy reveals normal glomeruli on light microscopy with some lipid in the PCT cells. What would you see on IF and EM? What would be the next step in care?
Minimal Change disease (lipoid nephrosis) - Triggered by recent infection, immunization or immune stimulus. May be associated with Hodgkin lymphoma.
IF - Negative
EM - Effacement of foot processes
Give CORTICOSTEROIDS - Excellent response
In minimal change disease all kinds of protein can be lost in the urine, True or False?
False
Selective proteinuria (loss of albumin but NOT immunoglobulin)
A patient has systemic amyloidosis, what is the most likely affected organ? What would biopsy reveal?
Kidney is most commonly involved. Associated with chronic conditions (e.g. multiple myeloma, TB, rheumatoid arthritis).
LM - congo red stain shows apple-green birefringence under polarized light
Compare and contrast the key differences between Type 1 and Type 2 Membrano-proliferative glomerulonephritis:
Type 1: Subendothelial IM complex deposits w/ mesangial ingrowth that gives “TRAM TRACK” apperance. Granular + IF. Associated w/ HBV/HCV or idiopathic.
Type 2: Intramembranous IC “DENSE” deposits. Associated w/ C3 nephritic factor auto-antibody.
Describe the immune process that results in Type 2 MPGN:
C3 nephritic factor auto antibody stabilizes C3 convertase, increasing formation of complement, leading to infection and subsequent glomerular damage
A 50 year old female diabetic patient presents with signs of nephrotic syndrome. A biopsy of the kidney is taken. What would you see on LM and what is the key process that leads to this pathology?
LM - Mesangial expansion, GBM thickening, and eosinophilic nodular blomerulosclerosis (Kimmelstiel-Wilson lesion)
Nonenzymatic glycosylation of GBM and preferentially the Efferent arteriole.
What are they key signs of NephrITic Syndrome?
this is an INflammatory process. Hematuria and RBC casts in urine.
Associated with azotemia, oliguria, hypertension (from salt retention) and mild proteinuria (<3.5g/day)
An 8 year old boy presents with mild fever, azotemia and periorbital edema. He produces a cola-colored urine sample which reveals RBC casts. There is also small amounts of proteinuria. A blood test reveals elevated levels of anti-DNase B titers and decreased compliment. His mother adds that he was very ill, with a bad cough, about 2 weeks ago. A kidney biopsy is taken, what would be seen on LM/IF/EM? What was the cause of his symptoms?
Acute poststreptococcal glomerulonephritis - Type III hypersensitivity reaction
LM - glomeruli enlarged, inflamed and hypercellular
IF - Positive “starry sky” granular appearance (IgG, IgM, C3 deposition along GBM and mesangium)
EM - Subepithelial immune complex HUMPS
A 23 year old male, who had acute poststrep GN, presents about a month after with rapidly deteriorating renal function and hematuria/hemoptysis. A kidney biopsy is taken and IF reveals a linear pattern. What would you see on light microscopy and what is the reason for this characteristic IF presentation?
Patient has Rapidly progressive glomerulonephritis (RPGN)
LM - Crescent - moon shape (consist of FIBRIN and MACROPHAGES)
IF is because patient has GOODPASTURE SYNDROME - type 2 hypersensitivity producing antibodies to GBM and alveolar basement membrane. This forms the characteristic line
A patient presents with Hemoptysis, Hematouria and sinusitis. A biopsy reveals cresent-moon shaped lesions in the glomeruli with negative IF. What should the next test be and what would it most likely reveal?
Patient has RPGN
Perform ANCA test
c-ANCA: Wegners granulomatosis
A patient with RPGN, granulomatous inflammation, eosinophilia and asthma presents. Biopsy also reveals negative IF. What does this patient likely have and what test confirms this?
Churg-Strauss diseaes
p-ANCA would confirm
w/o signs of granulomatous inflammation, eosinophilia and asthma, then patient has microscopic polyangitis
A 35 year old AA female presents with signs of azotemia, oliguria and hypertension. Urine sample reveals massive proteinuria, hematuria, and RBC casts in urine. A kidney biopsy is taken and IF is granular. What would LM reveal and what associated condition does this person likely have?
Diffuse proliferative glomerulonephritis due to SLE (LUPUS)
LM - “wire looping” of capillaries
A middle aged male patient presents following an upper respiratory tract infection, with signs of Nephritic Syndrome. Urine tests over two days reveal episodic hematuria with RBC casts. He has had similar episodes like this in the past and further tests reveal he may be developing renal failure. What would biopsy reveal for LM/EM/IF?
IgA nephropathy (Berger disease)
LM - mesangial proliferation
EM - mesangial IC deposits
IF - IgA-based IC deposits in mesangium
A young adult male patient presents with isolated hematuria, sensory hearing loss and ocular disturbances. He shows signs of glomerulonephritis. What is the most likely reason for this patient’s symptoms?
Alport Syndrome
X-linked inherited mutation of Type IV collagen, which causes thinning and splitting of GBM
A 62 year old man presents with unilateral flank tenderness, colicky pain radiating to his groin and hematuria. Urine tests show envelope shaped crystals and high calcium levels. Serum calcium is normal. What condition does this person have and what are conditions that can precipitate it? What Tx may prevent recurrence of this problem?
Calcium Oxalate stone from idiopathic hypercalciuria most likely
Conditions: Ethylene glycol, Vitamin C abuse, or Crohn Disease
Tx: Hydrochlorothiazide to decrease amount of Ca to urine
A 32 year old female presents with unilateral flank tenderness, colicky pain radiating to the groin, and hematuria. Urine analysis reveals Coffin Lid shaped crystals. The patient also has signs/sx consistent with a UTI. What condition does this patient most likely have and what would you find in her kidneys?
Ammonium magnesium phosphate kidney stone caused by infection with urease + bugs (Proteus mirabilis, staph, Klebsiella)
Staghorn Calculi in renal calyx (needs to be removed surgically)
A 43 year old man presents with sx consistent with a renal stone. He recently spent time vacationing in Arizona and has a history of gout. He is not producing much urine, and his urine has an acidic pH. What test do you want to do next? Treatment?
Uric Acid Stone - probably from hyperuricemia from gout
Do Ultra Sound and possibly a CT (XRay would not reveal)
Tx: Allopurinal for Gout, hydration and alkalization of urine with potassium bicarbonate
A young child comes in with signs/sx consistent with a renal stone. Imaging reveals staghorn colliculi, and sodium nitroprusside test is positive. Urinalysis reveals hexagonal crystals. What is the underlying cause of this disorder?
Cystine Stone
Cystinuria –> Genetic defect of tubules that results in decreased reabsorption of cysteine
What is hydronephrosis and how may it develop? What are some complications that may result?
Distention/dilation of renal pelvis and calcysis
Caused by: UT obstruction (stones, BPH, cervical cancer, injury to ureter) or from, retroperitoneal fibrosis and vesicoureteral reflux.
May lead to compression atrophy of renal cortex and medulla.
A 58 year old man presents with hematuria and flank pain. He has a 40 pack year history and is obese, although he has lost 20 pounds in the last 6 weeks. He has a left-sided varicocoele and a fever. What are some major associated syndromes this patient may have with primary disease? If a biopsy was taken, what would it reveal?
Paraneoplastic syndromes:
- EPO - reactive polycythemia
- Renin - HTN
- PTHrP - Hypercalcemia
- ACTH - Cushing syndrome
Biopsy: Renal Cell Carcinoma (primary renal malignancy), clear cell histology
Gross: Yellow mass
What is the pathogenesis of renal cell carcinoma and what are the two pathways that can lead to this?
Loss of tumor suppressor gene VHL (chromosome 3) –> increased IGF1 promotes growth –> increased HIF transcription factor –> increased VEGF and PDGF
Sporadic: single tumor in upper pole of kidney in adult smoker
Hereditary: Multiple bilateral tumors in a young patient
A middle aged patient presents with painless hematuria, flank pain, and signs of abdominal mass. The patient undergoes nephrectomy which reveals a well-circumscribed mass with a central scar. What would sample show on histology?
Renal oncocytoma
Histo: Large round/polygonal cells with granular eosinophilic cytoplasm and round nuclei, with abundant mitochondria without perinuclear clearing
A 3 year old boy presents with a huge palpable flank mass, hematuria and HTN. What would a biopsy of the mass reveal? What could this patients condition be associated with?
Wilms Tumor
Biopsy: blastema (small dark blue cells), primitive renal cells and primitive glomeruli, tubules and stromal cells
WAGR Syndrome - Wilms tumor, Aniridia, Genitoruinary anomalies, mental Retardation
A 65 year old female smoker presents with painless hematuria and no casts in the urine. She just retired from working as a hairdresser. Ultrasound reveals a mass in the bladder. What may biopsy show? What are associated causes for her condition?
Biopsy: Transitional cell carcinoma; papillary growth lined by transitional epithelium with mild nuclear atypia and pleomorphism
Associated with problems in your Pee SAC: Phenacetin, Smoking, Aniline dyes, and Cyclophosphamide
A 27 year old male presents with painles hematuria. He recently flew back to the US after serving some time for the US Army in the Middle East. Ultra sound reveals a mass in the bladder. What is the most likely cause of this disorder? What are other possible causes?
Squamous Cell Carcinoma - high risk from Schistosoma haematobium parasite infection
Other risks: Chronic cystitis, smoking, chronic nephrolithiasis
Develops from chronic irritation of urinary bladder leading to squamous metaplasia then dysplasia of these cells
A 22 year old female presents with suprapubic pain, dysuria, urinary frequency and urgency. She reports that she is sexually active. Urinalysis is cloudy with >10 WBCs/hpf, dipstick is positive for leukocyte esterase and nitrites, and culture shows >100k colony forming units. What is the most likely cause of her symptoms? If She had sterile pyuria, what would the cause likely be?
Acute infectious cystitis from E. Coli (staphlyococcus saprophyticus also very likely. Kebsiella and proteus (urine has ammonia scent) also possible.
Sterile Pyuria and negative urine cultures, suggests urethritis by Neisseria gonorrhoeae or Chlamydia trachomatis
A 26 year old sexually active female presents with dysuria, fever, costovertebral angle tenderness, nausea and vomiting. Patient has WBC casts in urine and CT shows striated parenchymal enhancement. What does this patient have and what part of the kidney are likely affected? What was this most likely caused by?
Acute pyelonephritis- possibly from ascending UTI, vesicoureteral reflux and hematogenous spread to kidney.
Affects cortex with relative sparing of glomeruli/vessels.
E. Coli is most often the cause
What key pathogenesis occurs in a patient who has recurrent episodes of acute pyelonephritis? What are risk factors for this condition?
Chronic pylonephritis
- Cortical scarring w/ blunted calyces at upper and lower poles of the kidney
- THYROIDIZATION of kidney - atrophic tubules contain Eosinophilic proteinaceous material
Vesicoureteral reflux or chronically obstrucuting kidney stones predispose to chronic infection.
A patient presents with fever, rash, hematuria and costovertebral angle tenderness. They show signs of acute interstitial renal inflammation, pyuria (w/ Eosinophils) and azotemia. What key followup information is required of this patient?
Drug-induced interstitial nephritis (tubulointerstitial nephritis) - hypersensitivity reaction
See if any particular drugs were taken 1-2 weeks ago (diuretics, penicillin derivatives, sulfonamides, or rifampin). Possibly NSAIDs from months back
If a pregnant woman undergoes obstetric catastrophe or is in septic shock, what may she be at risk of developing?
Diffuse cortical necrosis - Acute generalized cortical infarction of both kidneys
What is the most common cause of intrinsic renal failure and what are its key features?
Acute tubular necrosis
- Muddy brown casts in urine
- Azotemia (as with most acute renal failure)
- Decreased reabsorption of BUN and Na (BUN/Cr decrease, FENa >2%)
- Inability to concentrate urine
What are the two possible causes of acute tubular necrosis?
Ischemic - Decreased blood supply leads to death of tubular cells. Proximial tubule and thick ascending limb are highly susceptible to injury.
Nephrotoxic - Initial injury resulting from toxic substances (Aminoglycosides, radiocontrast agents, lead, cisplatin), crush injury (myoglobinuria), hemoglobinuria. Proximial tubule is susceptible.
A 50 year old diabetic patient presents with gross hematuria and proteinuria, following a recent infection. What may they have?
Renal papillary necrosis - sloughing of renal papillae
Also associated with: Acute pyelonephritis, chronic phenacetin use, sickle cell anemia and trait.
What are the consequences of Uremia?
Increased BUN and Creatinine
- Nausea/anorexia
- Pericarditis
- Asterixis (flapping tremor)
- Encephalopathy
- Platelet dysfunction
What are the main consequences of renal failure?
MAD HUNGER
Metabolic Acidosis Dyslipidemia (high triglycerides) Hyperkalemia Uremia Na+/H2O retention (CHF, pulmonary edema, HTN) Growth Retardation and developmental delay (children) Erythropoietin failure (anemia) Renal osteodystrophy
A patient on dialysis and in chronic kidney disease is found to have shrunken kidneys. What can you conclude about the state of their Kidneys?
they must have CYSTS
What are the three key components to Renal Osteodystrophy?
- Osteitis fibrosa cystica - Hypocalcemia –> increased PTH –> resorption of bones to increase Ca –> fibrosis and cysts form in the bones
- Osteomalacia - Cannot mineralize ostioid made by osteoblasts because of decreased vit. D fxn and subsequent decrease Ca
- Osteoporosis - Patient is in Metabolic Acidosis requiring buffer. Calcium leeched from bone over time to buffer.
A 22 year old male presents with flank pain, hematuria, HTN, urinary infection and progressive renal failure. Ultrasound reveals two very large kidneys. What is this patient suffering from and what are some issues associated with their disease?
Autosomal Dominant Polycystic Kidney Disease (ADPKD)
Associated with berry aneurysms, mitral valve prolapse, and benign hepatic cysts. High renin –> HTN can also be cause of death.
A neonate is presented with symptoms consistent with portal HTN and Potters sequence. The baby is experiencing worsening renal failure. What do they have?
Autosomal Recessive (Infantile) Polycystic Kidney Disease (ARPKD)
Bilateral, enlarged kidneys with cysts in renal cortex and medulla.
A patient presents with progressive renal insufficiency with the inability to concentrate urine. What would you see on ultrasound and biopsy??
Shrunken kidneys on US, medullary cysts not visualized.
Biopsy: Tubulointerstitial fibrosis
What is the difference between a simple and complex renal cyst?
Simple cysts on outer cortex and filled with ultrafiltrate. Very common and asymptomatic
Complex cysts can be septated, enhanced or have solid components seen on CT. Require removal due to risk of RCC.
What would be a drug of choice in a patient with drug overdose or increased intracranial/intraocular pressure? What are some of the risks and contraindications of using this drug?
Mannitol (osmotic diuretic) increasing tubular fluid osmolarity –> increased urine flow
Tox: Pulm edema, dehydration.
Contraindicated: Anuria, CHF
A patient has glaucoma, urinary alkalinization and metabolic alkalosis. What would be a drug of choice and what are its toxicities?
Acetazolamide (carbonic anhydrase inhibitor) causes self limited NaHCO3 diuresis and decrease total body carbonate
Tox: METABOLIC ACIDOSIS, paresthesias, NH3 tox, sulfa allergy
A patient presents with edema, HTN and hypercalcemia. What may be a drug of choice and what are its risks? How is this drug inhibited?
Furosemide (loop diuretic) inhibites Na/K/2Cl cotransporter preventing concentration of urine
Tox: OH DANG; Ototoxicity, Hypokalemia, Dehydration, Allergy, Nephritis, Gout
NSAIDs will inhibit its stimulation of PGE release (which normally would cause dilation of afferent arteriole)
What drug would you choose in a patient with sulfa allergy who requires diuresis? What is a major precaution in using this drug?
Ethacrynic Acid
causes hyperuricemia, NEVER USE IN GOUT
A patient presents with HTN, CHF, proteinuria and has a history of diabetic nephropathy. What would be the drug of choice and what are its risks?
ACE Inhibitor (Captopril, enalapril, lisinopril) - decreases angiotensin II, subsequent decrease GFR.
Tox: Captopril’s CATCHH; Cough, Angioedema, Teratogen (fetal renal malform.), increase Creatinine (decrease GFR), Hyperkalemia, Hypotension
AVOID in bilateral renal artery stenosis
A patient presents with extensive edema and signs of CHF. Patient also has hyperaldosteronism and serum potassium is low. What would be the drug of choice and what are the risks?
Potassium Sparing diuretic (the K+ STAys; Spironolactone/eplerenone, Triamterene, Amiloride); function at the level of collecting tubule
Tox: Hyperkalemia (lead to arrhythmias), endocrine effects w/ spironolactone (gynecomastia and antiandrogen)
A patient presents with HTN and signs of CHF. They have edema, and urine analysis shows hypercalcuria. What would be the drug of choice and what are its toxicities? (Hint: also used in cases of nephrogenic diabetes insipidus or osteoporosis)
Hydrochlorothiazide (thiazide diuretic) inhibits NaCl reabsorption in early DTC, decreasing Ca excretion and diluting capacity of nephron
Tox: HyperGLUC; hyperGlycemia, hyperLipidemia, hyperUricemia, hyperCalcemia
Also hypokalemic metabolic alkalosis, hyponatremia and sulfa allergy
