Nephrology Flashcards
Acute ↑ Cr, BUN/Cr > 20, U Na < 10, FE Na < 1%. Dx and next step?
AKI pre-renal etiology.
If dry (e.g., diarrhea, dehydration, hemorrhage) –> IVF.
If wet (e.g., third space: nephrotic syndrome, malnutrition, cirrhosis) –> diuretics.
Acute ↑ Cr, hydronephrosis or hydroureter. Dx, posible causes and next step?
AKI post-renal.
Posible causes: Neoplasia, Kidney stones, Neurogenic bladder, BPH
Next step: catheter, stent, surgery
Acute ↑ Cr, BUN/Cr < 10, U Na > 10, FE Na > 1%, RBC casts. Dx and next step?
AKI: glomerulonephritis.
Next step: Rule out nephrotic syndorme ( > 3.5 g/d of proteinuria, ↑ Cholesterol, edema)
Acute ↑ Cr, BUN/Cr < 10, U Na > 10, FE Na > 1%, muddy brown casts . Dx and posible causes?
AKI: acute tubular necrosis.
Caused by ischemia and toxins (IV constrast, myoglobin)
Acute ↑ Cr, BUN/Cr < 10, U Na > 10, FE Na > 1%, WBC casts, WBC, eosinophils. Dx and next step?
AKI: Acute interstitial nephritis
Can be cause by infections and reactions to drugs (trimetropim sulfa, penicillin, cephalosporins)
Which drugs may generate acute interstitial nephritis?
trimetropim sulfa, penicillin, cephalosporins
Acute indications for hemodialysis?
o A: Acidosis o E: Electrolites (K, Ca) o I: Intoxication o O: Overload o U: Uremia
Kidney anatomical anormality + GFR > 90. Stage of CKD and management?
Stage I.
Prevent progression
GFR 60-89. Stage and management?
Stage II
Prevent progression
GFR 30-59. Stage and management?
Stage III
Prevent progression, manage complications
GFR 15-29. Stage and management?
Stage IV
Prevent progression, manage complications, prepare for dialysis
GFR < 15. Stage and management?
Stage V, dialysis, transplant
Goals of BP in CKD.
BP < 130/80.
Tx of HTN in CKD?
Use ACEI or ARB
Goals of DM in CKD?
Goals: HbA1C <7; glucose < 80-120
Tx of DM in CKD?
Use oral meds (excepts for metformin) and/or insulin
Dx of anemia in CKD
Hb < 12
Dx of exclusion (look first for Iron, folic, B12)
No need to ask for EPO to diagnose
Goal of Hb in CKD?
HB > 10
Tx of secondary HyperPTH + Mineral Bone Disease (Osteopenia) in CKD?
- Phosphate binders (e.g., Sevelamer)
- Calcium mimetics (e.g., Cinacalcet)
- Ca + Vit D
Tx of volume overload in CKD?
Use loop diuretics (e.g., furosemide) +/- Thiazides (e.g., metolazone)
Na < 135, ASx. Tx?
Disease specific
Na < 135, nausea, vomiting, headache. Tx?
IV NS
Na < 135, coma, seizure. Tx?
IV hypertonic
Na > 145, ASx. Tx?
PO water
Na > 145, nausea, vomiting, headache. Tx?
IV NS
Na > 145, coma, seizure. Tx?
IV D5W
How to correct Na to prevent complications?
- A correction of 4 to 6 might be enough to treat Sx.
- Correct Na by 0.25/hr. If you correct to quick –> risk of osmotic demyelination syndrome (aka pontine and extra-pontine myelinolysis)
How to correct Na if glucose if high?
If hypertonic, for each 100 of blood glucose above
100, you add 1.6 to the Na
E.g., If Na is 130 and glucose is 500 (i.e., four 100s above 100), real Na = 130 + (1.6 x 4) = 136.4
Na < 135, ↓Osm, JVD, edema, CHF, anasarca. Next step?
Diuresis
Na < 135, ↓Osm, dry mocous, burns, fever, sepsis, hypotension
IV fluids (NS if moderate Sx, hypertonic if severe)
Na < 135, ↓Osm, normal volumen (aka, no edemas, no dehydration).
Possible Dxs?
R: Renal tubular acidosis –> Uroanalysis
A: Addison –> cortisol
T: Thyroid –> TSH
S: Sd. Inappropriate ADH –> Dx of Exclusion
Na < 135, ↑Osm. Next step?
Correct Na considering glucose levels
Na < 135, normal Osm. Dx?
PseudoHypoNa
Which medication is NEVER the answer to treat hypoNa?
Vaptans are never the answer to treat hypoNa!
Causes of Hyperkalemia
Low aldosterone (Meds: ACEI, ARB, aldo inhibitors)
Iatrogenic
Ingestion + CKD
CKD stage V
Most common: Artifact (hemolysis, fist squeezing during sample)
Hyperkalemia, changes in ECG?
Wide QRS
Picked T wave
Hyperkalemia workup?
Recheck K leves
Look for ECG changes
K levels high (confirmed) without ECG changes. Dx and next step?
Stable hyperkalemia
Next step: Kayexalate and stop ACEI, ARB, aldo inhibitors
K levels high (confirmed) with ECG changes. Dx and tx?
Unstable hyperkalemia
Tx:
- IV Ca: stabilize
- Insuline + glucose (D50): Shifts K into cells
- HCO3: Shifts K into cells
- Kayexalate: ↓ total body K
- Loop diuretis/dialysis: ↓ total body K
Causes of hypokalemia?
Renal loses
• HyperAldo (Conn’s, renal arthery stenosis, thiazides, loop diuretics)
• Check BP and ABG
GI loses (vomiting, diarrhea)
ECG changes in hypokalemia?
flattening of T waves, U waves, depressed ST segment
Hypokalemia workup?
Recheck K leves
Look for ECG changes
Repletion of K in hypokalemia
PO preferred (e.g., K-Dur)
If IV is chosen, don’t go faster than:
• Peripheral: 10 mEq/h
• Central: 20 mEq/h
Rate: 10 mEq change serum K by 0.1
If refractory hypokalemia?
if refractory, check Mg and replace it if low
Gold standard for kidney stones
NonCon CT (used on the first episode)
When to use KUB in kidney stones?
KUB (abdominal xR) is used to track the evolution and in subsequent episodes
Hematuria, colicky flanck pain that radiates to the groin. Next step?
U/A
Pregnant, hematuria, colicky flanck pain that radiates to the groin, U/A with hematuria. Next step?
Ultrasound
Stone < 5mm
IVF + NSAIDs
Stone < 7mm
IVF + NSAIDs + alpha blocker (prazosin) / CCB (amlodipine)
Stone at the kidney level < 2cm
Tx?
Extracorporeal shock wave lithotripsy (ESWL),
Stone at the kidney level > 2cm
percutaneous nephrolithotomy (PCNL)
Stone at the urether > 1 cm
Extracorporeal shock wave lithotripsy (ESWL), Ureteroscopy (URS), percutaneous nephrolithotomy (PCNL), laparoscopy
Stone at the bladder, refractory to med Tx
Cystolitholapaxy, ureteroscopy
Outpatient follow-up of kidney stone
Once stone is out –> determine the type of stone –> modify risk factors –> 6 weeks later, do a 24-hr urine –> if stones still present keep modifying factors, if not present, cured!
Hematuria, colicky flank pain that radiates to the groin., U/A with hematuria, KUB normal. Next step?
Take uric acid
Calcium oxalate kidney stone. How to treat risk factors?
Thiazides, ↓ meat, ↑fruit (don’t reduce the intake of calcium!!)
Bacteria resonsible for struvite stones
Proteus
Uric acid kidney stone. How to treat risk factors?
Allopurinol
Incidental finding of a small renal cyst with no loculation or septation. Next step?
No further workup of tx needed
Incidental finding of a large renal cyst with heterogenous structure. Next step?
U/A
CT scan (US if pregnant)
Bx
Complications of Complex renal cysts
pyelonephritis, pain, bleeding (hematuria)
Classic triad of renal cancer
Flank pain
Flank mass
Hematuria
Paraneoplastic sd of renal cancer
↓Hb
↑EPO Polycythemia
Trombus in IVC or DVT
Renal mass of neoplasic apearance. Next step and tx?
Workup: U/A, CT scan (US if pregnant), NO Bx
Tx: parcial or radical nephrectomy
Extra renal manifestations of Autosomal dominant poly-cystic kidney disease (ADPCKD)
- Hepatic cyst/hepatitis
- Pancreatic cyst/Pancreatitis
- Cerebral aneurism (Screen for berry aneurisms with magnetic resonance with angiogram/CT angiogram/angiogram)
- Diverticulosis
- Mitral valve prolapse
Presentation of Autosomal recessive poly-cystic kidney disease (ARPCKD)
- Anuria
- Renal failure
- Olygohydramnios
- Bilateral flank mases
- Perinatal death
pH < 7.4, CO2 > 40. Dx and next step?
Respiratory acidosis. Manage underlying conduction (hypoventilation) Opiates COPD Asthma OSA Muscle strength
pH < 7.4, CO2 < 40. Dx and next step?
Metabolic acidosis. Get Anion gap (Na-Cl-HCO3)
pH < 7.4, CO2 < 40, anion gap > 12. Dx and next step?
Anion gap metabolic acidosis. Treat underlying condition (MUD PILES): Methanol Uremia DKA Propylene Glycol Iron Lactic acidosis Ethylene glycol Salycilates
pH < 7.4, CO2 < 40, anion gap < 12. Dx and next step?
Non-anion gap acidosis. Get Urine anion gap (Na+K-Cl).
If (+) –> Renal tubular acidosis
If (-) –> Diarrhea
pH > 7.4, CO2 < 40. Dx and next step?
Respiratory alkalosis. Treat the underlying condition (hyperventilation):
Pain
Anxiety
Hypoxemia
pH > 7.4, CO2 > 40. Dx and next step?
Metabolic Alkalosis. Get urine Cl
pH > 7.4, CO2 > 40, urine Cl < 10. Dx and next step?
Volume-responsive Metabolic Alkalosis. Treat underlying condition: Diuretics Dehydration Emesis NG tube
pH > 7.4, CO2 > 40, urine Cl > 10. Dx and next step?
Not-Volume-responsive Metabolic Alkalosis. Check BP
If HTN –> Hyperadosteronism, renal artery stenosis, Cushing’s
If HTN –> Genetic diseases
What type of renal tubular acidosis (RTA) is associated with abnormal H+ secretion and nephrolithiasis?
Type I (distal) RTA.
Renal tubular acidosis associated with abnormal HCO3 – and rickets.
Type II (proximal) RTA.
Renal tubular acidosis (RTA) associated with aldosterone defect.
Type IV (distal) RTA.
“Doughy” skin .
Hypernatremia
Differential of hypervolemic hyponatremia.
Cirrhosis, CHF, nephrotic syndrome.
Chvostek’s and Trousseau’s signs.
Hypocalcemia.
The most common causes of hypercalcemia.
Malignancy and hyperparathyroidism.
T-wave fl attening and U waves. .
Hypokalemia
Peaked T waves and widened QRS.
Hyperkalemia.
First-line treatment for moderate hypercalcemia.
IV hydration and loop diuretics (furosemide).
Type of Acute kidney injury in a patient with FeNa < 1%.
Prerenal.
A 49-year-old man presents with acute-onset flank pain and hematuria.
Dx?
Nephrolithiasis.
The most common type of nephrolithiasis.
Calcium oxalate.
A 20-year-old man presents with a palpable fl ank mass and hematuria. Ultrasound shows bilateral enlarged kidneys with cysts. Associated brain anomaly?
Cerebral berry aneurysms (autosomal-dominant PCKD).
Hematuria, hypertension, and oliguria.
Nephritic syndrome.
Proteinuria, hypoalbuminemia, hyperlipidemia,
hyperlipiduria, and edema.
Nephrotic syndrome.
The most common form of nephritic syndrome.
Membranous glomerulonephritis.
The most common form of glomerulonephritis.
IgA nephropathy (Berger’s disease).
Glomerulonephritis with deafness.
Alport’s syndrome.
Glomerulonephritis with hemoptysis.
Wegener’s granulomatosis and Goodpasture’s syndrome.
Presence of red cell casts in urine sediment.
Dx?
Glomerulonephritis/nephritic syndrome.
Eosinophils in urine sediment.
Allergic interstitial nephritis.
Waxy casts in urine sediment and Maltese crosses (seen with lipiduria).
Nephrotic syndrome.
Drowsiness, asterixis, nausea, and a pericardial friction rub.
Uremic syndrome seen in patients with renal failure.
A 55-year-old man is diagnosed with prostate cancer.
Treatment options?
Wait, surgical resection, radiation and/or androgen
suppression.
Low urine specific gravity in the presence of high serum osmolality.
Diabetes insipidus.
Treatment of SIADH?
Fluid restriction, demeclocycline.
Hematuria, flank pain, and palpable flank mass.
Renal cell carcinoma (RCC).
Testicular cancer associated with β-hCG, AFP.
Choriocarcinoma.
The most common type of testicular cancer.
Seminoma, a type of germ cell tumor.
The most common histology of bladder cancer.
Transitional cell carcinoma.
Complication of overly rapid correction of hyponatremia.
Central pontine myelinolysis.
Salicylate ingestion occurs in what type of acid-base
disorder?
Anion gap acidosis and 1° respiratory alkalosis due to central respiratory stimulation.
Acid-base disturbance commonly seen in pregnant women.
Respiratory alkalosis.
Three systemic diseases that lead to nephrotic syndrome.
DM, SLE, and amyloidosis.
Elevated erythropoietin level, elevated hematocrit, and normal O2 saturation suggest?
Renal Cell Cancer or other erythropoietin-producing tumor; evaluate with CT scan.
A 55-year-old male presents with irritative and obstructive urinary symptoms. Treatment options?
Likely BPH. Options include no treatment, terazosin,
fi nasteride, or surgical intervention (TURP).
Patient who on POP day 1 of thyroidectomy/parathyroidectomy develops Tetany, Perioral tingling, Trousseau sign and Chvostek sign
- ↓PTH
- ↓ionized Ca
Dx and tx?
Iatrogenic HypoPTH
Tx: IV calcium (gluconate or carbonate)
Patient with
• ↑PTH
• ↓Ca
• ↑P
Dx?
PseudoHypoPTH
PTH insensitivity
Patient with osteopenia with dexa scan -2.0.
Possible dx and Next step?
Vitamin deficiency
Next step: ↓ 25 Vitamin D (< 30)
Tx: Ca + vit D
• Add bisphosphonates if severe osteopenia
Patient with early stage CKD and hypoCa.
Dx and Tx?
Secondary hyperPTH: ↓VitD production leads to HypoCa. Therefore ↑PTH is secreted (secondary hyperPTH).
Tx:
• Ca+VitD
• Cinecalcet (to decrease PTH and prevent tertiary HyperPTH)
Patient at the internal medicine floor. The nurse says that the patient has low Ca.
Next step and tx?
Next step:
- Albumin (correction of albumin corrects Ca)
Tx: If Ionized calcium remains low, IV calcium (gluconate or carbonate)
Patient with Altered mental status (psychic moans), Abdominal pain (abdominal groans).
↑↑ Ca
Next step?
- lots of IVF + early bisphosphonates
- If really high Ca and super Sx patient: Calcitonin
Patient with Pathologic fractures, ↓Bone density. On Rx Brown tumor in a bone.
- ↑PTH
- ↑Ca
- ↓P
Dx and next step?
HyperPTH
Next step: Sestamibi scan (nuclear Rx) to see parathyroid glands.
Patient with Pathologic fractures, ↓Bone density. On Rx Brown tumor in a bone.
- ↑PTH
- ↑Ca
- ↓P
- Sestamibi scan (nuclear Rx) shows a single big parathyroid gland, the other three are very small
Dx and Tx?
Autonomous adenoma producing Primary HyperPTH
Tx: Resection
Patient with CKD, Pathologic fractures, ↓Bone density. On Rx Brown tumor in a bone.
- ↑PTH
- ↑Ca
- ↓P
- Sestamibi scan (nuclear Rx) shows 4 big parathyroid glands
Dx and Tx?
autonomous multiple adenomas as a normal response to chronic hypoCa in CKD (tertiary HyperPTH).
Tx: resection
How are Ca, PTH and P in metastatic disease of the bone?
o ↑Ca
o ↑P
o ↓PTH
Patient with a mass in lung.
o ↑Ca
o ↓P
o ↓PTH
Dx and next step
Small cell carcinoma and Paraneoplastic syndrome
Next step:
o ↑PHT-rp (related pepetide)
Patient with Granulomatosis (TB, sarcoid).
• ↑Ca
• ↑P
• ↓PTH
Dx and Next step?
Hypervitaminosis D
Next step: • ↑1,25 Vitamin D
Patient with dx of primary hyperparathyroidism who had surgery. After the surgery he develops Perioral tingling, Trousseau sign, and Chvostek’s Sign.
Dx and tx?
Post-op hypocalcemia (the other glands are atrophied)
Tx: IV Ca++