Renal Flashcards
Whats on ddx when patient has Hypokalemia, Alkalosis, Normal BP
Low Urine Chloride
1. Bulimic (surreptious) vomiting
High Urine Chloride
- Diuretic abuse
- Bartters syndrome (reab defect in TAL NaK2Cl)
- Gittelmans syndrome (reab defect of NaCl in DCT)
Hyponatremia with Serum osmolality >300
Glucose, Mannitol, Contrast Agents
Hyponatremia with low serum Osm and Urine osm >100
SIADH
hypothyroid
glucorticoid def
drugs
Hyponatremia with low serum Osm and Urine osm <100
Primary polydipsia, Beer drinker potomania
Hyponatremia in schizophrenic patient
Psych hx –> Primary polydipsia
T/F: Hypercoagulation is commonly seen in nephrotic syndrome
True, especially renal vein thrombosis
->loss of Antithrombin III, changes to protein C and S, liver make more fibrinogen,
Earliest sign of diabetic nephropathy?
Glomerular hyperfiltration
Ultimately leads to GBM thickening, mesangial expansion, and the characteristic nodular sclerosis
Nephrotic syndrome in blacks/mexicans
FSGS
Nephrotic syndrome in heroin users, HIV, sickle cell, obesity
FSGS
Nephrotic syndrome in whites
Membraneous
How to remember nephrotic syndrome in whites vs blacks/mexicans
Blacks/Mexicans are segregated: FSGS
Whites are always members: Membraneous
T/F: Amitryptiline has anticholinergic side effects, including urinary retention
True. This TCA drug, used for pain/neuropathy, can cause atropine like sxs: dry mouth, urinary retention, etc.
Intramembraneous deposits that stain for C3 + proteinuria
Membraneoproliferative glomerulopathy
- -> caused by persistent activation of alternate pathway
- ->IgG Ab = C3 nephritic factor
Renal vascular lesions seen in hypertension
Arterio sclerotic of afferent and efferent arterioles and glomerular capillary
Characteristics of diabetic nephropathy
increased extracellular matrix, BM thickening, mesangial expansion, fibrosis
T/F: Diabetic nephropathy is characterized by nodular (or sometimes diffuse) glomerulosclerosis and GBM thickening
True, with Kimmelstiel-Wielstein lesion
Envelope-shaped rectangular crystals on UA
Calcium stones
- -> acidic low pH = calcium oxalate
- ->basic high pH = calcium phosphate
–Tx = hydration, thiazides, citrate
Causes of calcium oxalate stones (acidic low pH)
Ethylene glycol (antifreeze)
vitamin C abuse
malabsorption (Crohns)
Oliguria, hypertension, increased Creatinine/BUN a few days after renal transplant
Renal transplant dysfunction: causes = ureteral obstruction (look for dilated calcyces), cyclosporine toxicity (high levels), vascular obstruction, ATN, acute rejection
–>Acute rejection Tx with IV STEROIDS
How do you prevent contrast-induced nephropathy?
Pre-tx with IV hydration is the big one. can also pretx with sodium bicarb. can give acetylcysteine on top of one of those.
Signs of aspirin toxicity
Gastric ulcer, tinnitus. Causes hyperventilation and mixed respiratory alkalosis and anion gap metabolic alkalosis
T/F: Thiazides decrease uric acid
False. Toxicity can cause hyperuricemia
Tx for uric acid stones
Alkalinization of the urine (POTASSIUM CITRATE), low-purine diet, hydration. Or Allopurinol.
Hematuria, unilateral flank pain, palpable renal mass in a smoker
Renal cell carcinoma
best imaging for renal cell carcinoma?
abdominal CT
why might RCC present with polycythemia?
paraneoplastic EPO. can also have paraneoplastic ACTH, PTHrP
hyperaclcemia, thrombocytosis, erythrocytosis
Patient has hyperkalemia and ECG changes (no p waves, wide QRS, bradycardia). Mgmt?
So need the Calcium Gluconate first now.
After you can give the measures to decrease K
(Insulin = temporary; then Dialysis/cation exchange = perm)
Hyalinosis of afferent and efferent arterioles
Diabetic nephropathy (pathognomonic)
Patient with rheumatoid arthritis that develops nephrotic syndrome
strongly consider Amyloidosis
Urine sediment microscopy shows no or few rbcs, but UA shows large amounts of blood
Rhabdomyolysis secondary to myoglobulinuria
standard UA can’t distinguish btwn myoglobin and hemoglobin
What metabolic state would you expect after a seizure?
Anion Gap Metabolic Acidosis
- ->postictal rise in Lactic Acid (due to skeletal mm hypoxia)…self-resolves in about 2 hours
- ->esp seen with GTC seizures
wbc casts on UA
Pyelonephritis and Interstitial Nephritis (i.e. AIN)
broad and waxy casts on UA
Chronic renal failure
Fatty casts on UA
Nephrotic syndrome
Muddy brown granular casts on UA
ATN
What kind of casts on UA would you expect to see after MVA/hypovolemic shock?
Muddy brown –> ATN
What is ADPKD associated with?
Berry aneurysms (intracranial bleeding), MVP, benign hepatic cysts
Hypertension, bilateral palpable flank masses, microhematuria
ADPKD
electrolyte effects of Addison’s dz
= Primary Adrenal Insuff –> no Aldosterone.
Aldosterone normally saves sodium, secretes K and H+.
Addisons–>Hyponatremia, Hyperkalemia, non-gap metabolic acidosis
How do you use Winter’s formula?
arterial pCO2 should = 1.5 (HCO3) + 8…+/- 2.
So use this whenever trying to figure out what normal respiratory compensation is. based on this, you determine if there is respiratory disorder or appropriate compensation
How do you differentiate btwn glomerular and non-glomerular hematuria using UA?
Glomerular: Blood + Protein; rbc casts, dysmorphic rbc
(even if they say 3+ protein, don’t think “glomerulonephritis means less than 2+ protein…the bleeding still from glomerulus)
Nonglomerular: Blood + no protein, normal rbc
Hematuria/proteinuria after strep throat
Within 5 days: IgA nephropathy
Around 2 weeks: PSGN
don’t be a peasant kid
acid-base changes from Loops
Hypokalemia, Metabolic alkalosis, Pre-renal kidney injury (not called AKI, b/c this typically causes hyperkalemia and AG metab acidosis)
which dzs results in hyper-oxaluria and predisposes to stones?
Crohns or any malabsorption disorder.
oxalate is obtained from diet; normally bound by calcium in gut and absorption prevented. in fat malabsorption, calcium is bound to fat and leaves oxalate open.
causes of AIN (wbc casts, eosinophils in urine)
Drugs: Penicillin, Bactrim, Cephalosporins, NSAIDs
Features of AIN (wbc casts, eosinophils in urine)
Maculopapular rash (don’t pick gonorrhea), Fever, New drug exposure i.e. bactrim/nsaid/ABx +/- arthralgias
most common renal malignancy in childhood
Wilms (does not cross midline)
What is the biggest association with Wilms tumor?
BECKWIDTH-WIEDMANN
cancer in the 1st year of life, presents as abdominal mass that crosses midline with systemic sxs
Neuroblastoma (SNS chain; typically involves adrenal glands)
Who gets renal cell carcinoma?
Men 50-80 years old
What is the etiology of Hypernatremia?
Renal or GI losses (of water)
(less common: can be hypervolemic hypernatremia if excess sodium intake or mineralicorticoid excess from hyperaldosterone)
Hematuria with normal rbc suggests: (general)
extra-glomerular pathology i.e. not GN
T/F: Sickle cell trait patients can have spontaneous painless hematuria, UTI and renal medullary cancer
True, hematuria secondary to renal papillary necrosis/ischemia
common causes of metabolic alkalosis
- Vomiting!!!!
- Meds (thiazides/loops)
- Hyperaldosteronism (Hypokalemia)
whats the relationship btwn aldosterone and potassium
Normally, aldosterone saves sodium by pushing out K and H+(distal renal tubule).
- ->Aldosterone def: Hyperkalemia
- ->Aldosterone excess: Hypokalemia
Acid base status of Addisons dz (note: can be caused by TB in endemic areas, autoimmune or mets)
Primary Adrenal Insuff: Low Cortisol/T/ALDOSTERONE
–> Kidney loses sodium and retains K and H = Normal gap metabolic acidosis + Hyperkalemia and Hyponatremia
Tx of choice for hypovolemic hyponatremia
Normal Saline (replenishes depleted salt stores, restores euvolemia, shuts off nonosmotic stimuli for ADH release)
T/F: Protein and gross blood are present in both glomerular and non-glomerular hematuria
False.
Glomerular: Protein + Microscopic blood (dysmorphic)
Non-glomerular: Gross blood, no protein (normal rbcs)
causes of non-glomerular hematuria
Nephrolithiasis Cancer (RENAL/prostate/bladder) ADPKD Infection (cystitis) RENAL Papillary Necrosis
Most common glomerulonephritis in adults
IgA Nephropathy…5 days after URI or pharyngeal illness
causes of Renal Papillary Necrosis
Nsaids Sickle cell Analgesics Infx DM
Whats the major cause of refractory hypokalemia (despite trying to aggressively replenish K, level does not increase significantly)?
Hypomagnesemia (leads to excessive renal loss)
features of drug-induced interstitial nephritis (AIN)
- Fever, Rash, Arthalgia, Hematuria
- Sterile pyuria + Eosinophiluria. can have wbc casts
tx for drug-induced interstitial nephritis
remove offending agent habibi
flank pain and +urinary cyanide nitroprusside test
Cystinuria: Hexagonal crystals, impaired amino acid transport (Cystine, Ornithine, Lysine, Arginina aka COLA); radioopaque
Why does a patient with severe liver cirrhosis have decreased UOP despite resuscitative fluids?
Hepatorenal syndrome: systemic and renal hypoperfusion (NO in splanchnic circulation causes vasodilation). Patients have ARF with low Urine sodium (<10) and absence of casts, blood or protein in urine
Hyponatremia with low serum Osm (<280), high urine Osm (>100), and elevated Urine Na (>40)
SIADH
Drugs implicated in SIADH
SSRIs Carbamazepine NSAIDs Cyclophosphamide Sulfonylureas
Protocol for investigating VUR post febrile UTI’s in peds
First febrile UTI 2mo-24mo: Renal US (eval for anatomic abnormal)
Second/recurrent UTI: Voiding cystourethrogram (eval for VUR)
Dietary recommendations for patients with renal calculi
- Decrease sodium
- normal calcium
- lots of fluids
- increase citrate (fruits/veggies. Potassium citrate alkalinizes urine, good for uric stones etc)
leading cause of death in ESRD/dialysis patients
CVD son
Why does lymphoma patient getting treatment have arrythmia and EKG changes?
Tumor Lysis Syndrome –> Hyperkalemia
Treatment in hyperkalemia to stabilize cardiac membranes
Calcium carbonate
Treatment to rapidly lower serum potassium in a patient with hyperkalemia and EKG changes
you need to Temporize!
Give Insulin and Glucose (the calcium carbonate is to stabilize cardiac mem). This lowers SERUM k…vs kayexolate which decreases total potassium
Is there a difference between decreasing serum K and decreasing total body K in the treatment of a patient with hyperkalemia?
Yup!
Decrease serum K: Insulin and Glucose (hide it intracellularly)
Reduce total body K: Kayexelate (rids via stool). can also use Loops (urine) but not as common
What other options on top of Insulin/Glucose exist for rapidly decreasing serum K in a hyperkalemic patient?
- beta 2 agonists
- sodium bicarbonate (NaHCO3)
EKG changes of hyperkalemia
Prolonged PR interval Wide QRS interval PEAKED T WAVES loss of p wave Worse: can go to a sine wave
How do you do a UA/culture in a patient in diapers? i.e babies/elderly
Straight catheterization (avoid clean-catch, which is appropriate for majority of patients, b/c skin and stool flora contaminants)
what are the indications for dialysis
Acidosis (pH <7.1 refractory to medical tx)
Electrolytes (hyper K)
Ingestions (methanol, ethylene glycol, salicylate, Li, sodium valproate, carbamazepine)
Overload (V)
Uremia (encephalopathy/asterixis, pericarditis, bleeding)
Toxicity of thiazides (chlorthalidone/HZT)
- hypokalemic metab acidosis
- hyponatremia
- HYPER GLUC: Glycemia, Lipidemia, Uremia, Calcemia
options for removal of total body K in hyperkalemics
Kayexelate (med ed)
Diuretics (CI in ESRD pts)
Cation exchange resins (i.e. sodium polystyrene sulf)
Hemodialysis
How do you manage post-ictal lactic acidosis?
Observe and recheck in a few hours. Transient AG metabolic acidosis that resolves in 90 minutes
most common kidney stones
Calcium oxalate (radioopaque)
which stones are radioopaque?
Calcium and Ammonium Magnesium Phosphoate (aka Struvite). visible
features of cyanide toxicity (secondary to nitroprusside)
HA, confusion, AMS, arrythmia, flushing, respiratory depression
T/F: AIN typically presents with leukocyte casts/eosinophils, hematuria, and a RASH
True RASH
Most common cause of obstructive uropathy
BPH. Postrenal azotemia
best way to screen diabetics for development of nephropathy?
Spot (random) or time measurement of urine microalbumin to creatinine ratio (all about the MICROALBUMINURIA…so looking at creatinine clearance is the wrong answer)
T/F: Squamous cell lung cancer causes SIADH
False. SMALL CELL
Why does patient that comes in vomiting have low chloride?
Vomiting = Hypochloremic Hypokalemic Metabolic Alkalosis = GI LOSSES. CL, K, and H all present in gastric contents
In which 3 patients should you stop/not use Metformin?
Acute Renal Failure, Liver failure, Sepsis
Hypertension, Bilateral palpable flank masses and microscopic hematuria in a 50 year old
ADPKD…watch out for intracranial hem (Berry aneurysm leading to SAH). Hepatic cysts are actually most common extra renal manifestation. colonic diverticula and MVP/AR can also happen.
Leading cause of euvolemic hypernatremia
Diabetes Insipidus (SIADH is HYPOnatremia)
Increased thirst, polyuria, mild hypernatremia
Diabetes Insipidus. Inability to concentrate the urine b/c lack (central) or failure to respond (nephrogenic) to ADH
causes of central diabetes insipidus
Pituitary tumor, trauma, hemorrhage, infx
causes of nephrogenic diabetes insipidus
- Hypercalcemia
- severe hypokalemia
- meds: Lithium, Demeclocycline (ADH antagonist used in SIADH), Amphotericin, foscarnet/cidofivir (both for CMV retinitis, acyclovir-resistant HSV)
serum osm diff in central vs nephrogenic DI
Central <300 (closer to 100)
Nephrogenic: >300 (300-600)
Drug therapy that can help reduce nephrolithiasis
- calcium stones: Thiazides
- Uric acid: Allopurinol
- Urine alkalinization by Potassium Citrate
Why does patient with 4+ proteinuria have renal vein thrombosis (sudden development of pain)
Hypercoaguble state in nephrotic syndrome due to loss of Antithrombin III
Increased extracellular matrix, mesangial expansion, fibrosis, BM thickening of renal arterioles
Diabetic Nephropathy
Intimal thickening and luminal narrowing of renal arterioles with sclerosis
Arteriosclerotic lesions secondary to hypertension Habibi
Potassium sparing diuretics
Spironolactone, Epelrenone, Triamterene, Amiloride
–>potassium high when he EATS bananas
Papillary Necrosis and Tubulointerstitial Nephritis are caused by:
Analgesic-induced Nephropathy (chronic back pain patient on opioids/nsaids/etc)
–>painless hematuria, sterile pyuria, wbc casts, trace proteinuria
T/F: US is the best initial test for kidney stones
False! First get UA obvi but best test is NON-CONTRAST CT!!! Pregnant patients get US
how is a KUB used in dx of kidney stone?
Not used for Dx!!! Can be used to track dz progression of a known stone
Size rules for tx of stone
<5mm: passes spontaneously. Just fluids/pain meds
<7mm: medical CCB (Amlodipine), Alpha blocker (-zosin)
<1.5cm: break stone down… lithiotripsy (proximal) or ureteroscopy (Distal)
>1.5cm: Surgical resection (ex lap)
if ever SEPTIC: emergent decompression with Nephrostomy (proximal) or Stent (distal)
Patient comes in with bones, stones, groans, psychic moans. Management?
Hypercalcemia, first thing to do is VOLUME VOLUME VOLUME VOLUME VOLUME VOLUME. can augment with Calcitonin (short term/quick) and furesomide and BISPHOSPHENATES (long term)
Brown tumors/fibrosa cystica. Dz and mgmt
Primary hyperparathyroidism (hypercalcemic state). Single autonomous gland secreted PTH w/o feedback
- ->resection (after radionucleotide scan to ID which gland)
- ->monitor for hypocalcemia after surg
Why does early renal failure lead to secondary hyperparathyroidism?
Vit D not converted to active form = hypocalcemia = increased PTH (and hypertrophy)
Why does persistent renal failure lead to tertiary hyperparathyroidism?
Hypertrophied, autonomous parathyroid glands (initially hypertrophy due to vit d deficiency 2ndary hyperPTH)
How does imaging differentiate primary vs tertiary hyperparathyroidism
Sestamibi scan!
1: One huge gland
3: all the glands have some hypertrophy
weight loss, decrease PTH, increase Ca, increase P
bone mets (or granuloma…look for increase vit d)
weight loss, decrease PTH, increase Ca, decrease P
squamous cell, PTHrP
T/F: You order 1,25 vit D to see if granulomatous dz, you order 25, vit D in Vit D deficiency
true
Increase PTH, decreased Ca and decreased P
Pseudohypoparathyrodisim: PTH end organ resistance (low yield)
flank pain, flank mass, hematuria
likely cancer (RCC)
Why do nephrotic syndrome and cirrhosis lead to prerenal AKI?
Decreased albumin = third spacing
How do fibromuscular dysplasia and renal artery stenosis lead to prerenal AKI?
“Clog” = narrowing of vessels = decreased perfusion
Drugs that cause AIN
nsaids, bactrim, PCN, cephalosporins
how do you assess/rule out a postrenal obstruction?
US!!!! better than CT usually. Tx with foley/stent/remove obstruction/nephrostomy
what’s the creatinine level where you begin to dialyze?
NOT BASED ON Cr. AEIOU bruh
Hemoptysis, Hematuria, rbc casts, +Anti-basement membrane with linear deposits
Goodpastures. Tx with plasmapharesis and steroids
Sinusitis/otitis, lung problems, renal involvment with rbc casts + random systemic vasculitis signs
Wegeners. Tx with cyclophosphamide and steroids
Joint paint, purpuric lesions, +Hep C with renal involvement, high levels immunoglobulins
Cryoglobulinemia. Tx the Hep C with interferon, ribavirin, and protease inhibitor (-vir)
Tx of lupus nephritis
steroids, mycophenolate mofetil
Asthma, hematuria, eosinophils
Churg strauss. Tx with steroids, cyclophosphamide
Tx for secondary hyperparathyroidism
due to early renal failure and not converting vit d. Give phosphate binders (sevelamer) and calcimimeics (cinacalcet…sensitizes CaSR) . Can also give vit d and ca supplements
does CKD results in alkalosis or acidosis?
Acidosis (i.e. lactic acidosis). give bicarb supplement in CKD. also not saving sodium and swithcing with K/H
Synchronized vs unsynchronized cardioversion?
Synchronized = shock –> use for any tachyrrythmias (narrow/atrial or wide/ventricular) w/hemodynamic instability.
Unsynchronized = defribillation –> for pulseless cardiac arrest = VFIB, pulseless VTach
