Nephrology pearls

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Acute Kidney Injury

Formerly known as Acute Kidney Injury

Criteria

Rapid decline in renal fx, increase in Cr by 50% or from 0.5 1.0 or greater

Diagnostic Clues: Pulmonary and peripheral edema, dyspnea, decreasing urine output. Labs values - rising BUN, creatinine, and potassium

Causes: pre-renal, intrinsic or post-renal

A) Pre-renal: decrease in renal blood flow (60-70% of cases, most common); oliguria

is always present along with an increased BUN:Cr ratio of > 20:1

Absolute decrease in blood volume – bleeding, dehydration, burns, GI losses

Relative decrease in blood volume – CHF, sepsis, liver failure, anaphylaxis

Fractional Excretion of sodium FENa < 1% because the kidney is reabsorbing all Na to preserve volume (common pimping question – make sure you know what your patient’s FENa is and what it means)

FENa = [(U Na/P Na)/ (U Cr/P Cr)] x 100; U= urine, P= plasma

In patients on diuretics, the FENa may be > 1 even if ARF is secondary to pre-renal cause as the urine sodium will be elevated due to the diuretic.  In this case, the FEUrea can be helpful.

FENa most useful if pt is oliguric.

B) Intrinsic: damage to renal parenchyma (25-40% of cases)

Acute tubular necrosis:  ischemia from hypotension; nephrotoxic antibiotics (gent, ampho); IV contrast agents; heavy metals; globs of stuff sludging in the tubules (rhabdomyolysis, myeloma, amyloid, oxalate, uric acid, amino acid crystals); FENa > 2-3% b/c parenchyma damage is such that kidneys are unable to concentrate urine effectively, decreased BUN:Cr ratio < 20:1 and muddy brown casts are usually present.

AIN:  drugs (e.g., NSAIDs, antibiotics)

Acute glomerulonephritis

Vascular:  CVD, vasculitis, malignant hypertension

C) Post-renal

Urinary tract obstruction usually bilateral (5-10% cases, least common); increased tubular pressure such that urine formed cannot be excreted though blood supply and parenchyma are intact.  

Best tests to dx- physical exam palpate bladder, U/S look for obstruction/hydronephrosis and catheter placement (look for urine)

BPH urethral obstruction, most common cause

Stones – uric acid stones are the radiolucent ones, struvite are infected by Proteus (elevated urine pH)

Tumors of GU tract

Treatment

Supportive care—correct fluid imbalance and electrolyte disturbances, avoid further NSAIDs (decrease renal blood flow) and nephrotoxic medications, adjust med doses for kidney fxn, treat underlying problem

If severe, may require dialysis

Indications for acute/emergent Dialysis (AEIOU)

Acidemia (check that pH!)

Electrolyte imbalance (hyperkalemia)

Intoxicants/drugs/toxins

Overload of volume

Uremia, especially when mental status changes or uremic pericarditis present

Chronic Renal Failure/Chronic Kidney Disease

Irreversible, progressive decrease in GFR occurring over months or years; clinical measure of GFR by Cr Clearance with increasing Cr level associated with decreasing renal fxn

Causes- DM is most common, HTN second most common; 

other causes include chronic glomerulonephritis, interstitial nephritis, polycystic kidney disease or any cause of ARF that is not effectively treated

Clinical Features- HTN 2/2 salt and water retention from low GFR activating renin-angiotensin-aldosterone system, CHF from volume overload, anemia 2/2 decreased EPO production.  

Uremia may cause pericarditis, nausea, vomiting, anorexia, platelet dysfunction leading to bleeding.  

Neurologic symptoms include lethargy, somnolence and uremic seizures.  

Calcium-phosphorus disturbances usually manifest as hypocalcemia and hyperphosphatemia d/t secondary hyperparathyroidism.

Diagnosis- measure Cr clearance to est. GFR; severity depends on GFR—mild 70< GFR <120, moderate 30< GFR <70, severe GFR< 30, ESRD GFR< 10.  

Also do U/A, CBC, CMP and renal U/S to r/o obstruction and evaluate size of kidneys.

Treatment- Low protein, low salt diet.  ACE inhibitors reduce risk of progression to ESRD.  Strict BP control, glycemic control and correction of electrolyte abnormalities.  ESRD—dialysis and transplantation. 

Nephrolithiasis

Stones within the urinary tract most commonly found at the ureterovesicalar junction

Presentation- sudden onset colicky flank pain that radiates into the groin (pt writhes with excruciating pain), hematuria, N/V, UTI

Risk Factors- low fluid intake, fam hx, male gender, freq UTIs, medications (loop diuretics, acetazolamide, antacids), predisposing condition (gout, Crohn’s dz, hyperparathyroidism)

Types of stones- 

a) Calcium: most common (80%), radiodense on abd X-ray; usually 2/2 hypercalciuria, hyperoxaluria

b) Uric acid: 2nd most common (10%), require CT, U/S for dx; usu. 2/2 gout or chemotherapy tx  release of purines from dying cells causing increased uric acid levels

c) Struvite or staghorn stones: seen on abd X-ray; usu. 2/2 recurrent UTIs caused by urease producing bacteria (Proteus, Klebsiella, Serratia, Enterobacter spp)

Course- if stone > 1cm, will not pass spontaneously.  Stones < 1cm usually do pass spontaneously.  Recurrence is common within the next 10 years.

Treatment- IV morphine, vigorous fluid hydration, antibiotics if concurrent UTI; often can be managed as outpt—admit if pain not controlled by po meds, anuria, renal colic plus UTI/fever, large stone >1 cm.  For large stones consider extracorporeal shock wave lithotripsy or percutaneous nephrolithotomy.

Acid-Base Disorders:  

Normals pH 7.35-7.45, pCO2 35-45, pO2 80-100, HCO3 22-26

Metabolic Acidosis: pH low, plasma bicarb low

Diagnostic Clues:  tachypnea, abdominal pain, other symptoms depend on cause; elevated anion gap, ([Na+] – ([Cl-] + [HCO3-]) should be 12+4

Expected compensation: drop in pCO2 = 1.25*HCO3, 

(also pCO2 = last two digits of pH)

Causes: 

Anion Gap acidosis:  MUD PILES

  • Methanol
  • Uremia
  • DKA
  • Paraldehyde
  • Intoxication
  • Lactic acidosis
  • Ethylene glycol 
  • Salicylates (aspirin)
  • *Another mnemonic is MULE PAK:  Methanol, Uremia, Lactic acidosis, Ethylene glycol, Paraldehyde, Aspirin, Ketoacidosis

Non-gap acidosis:  glue sniffing, diarrhea, renal tubular acidosis, hyperchloremia (from IV fluids)

Treatment:  ABC’s, supportive care, find and treat underlying cause

Metabolic alkalosis: pH high, plasma bicarb high

Diagnostic Clues:  hypopnea, cyanosis, irritability, arrhythmias

Expected correction factor:  increase in pCO2 = 0.75* HCO3

Causes: 

Saline responsive (urine chloride < 10 mEq/L):  GI H+ losses (NG suction, emesis), very common cause is diuretics due to bicarb retention, hypovolemia

Saline resistant (urine chloride > 20 mEq/L):  hyperaldosteronism, Cushing’s syndrome, renal artery stenosis, severe hypokalemia or hypomagnesemia

Treatment:  for all causes provide supportive care, find and treat underlying cause

Saline responsive:  give saline

Saline resistant:  may use spironolactone or amiloride to counter mineralocorticoid excess

Respiratory acidosis: pH low, pCO2 >40

Diagnostic Clues:  agitation, headache, somnolence, papilledema, hypertension, tachycardia, cardiac arrhythmias

Expected correction factors:  

Acute respiratory acidosis: increase in HCO3 = 0.1*pCO2 

Chronic respiratory acidosis: increase in HCO3 = 0.4*pCO2

Causes: CNS depression from drugs, infection, brain injury; obesity; neuromuscular disorders like myopathies, Guillain-Barre, myasthenia; pulmonary diseases like COPD, sleep apnea, asthma, pneumothorax; kyphoscoliosis

Treatment:  correct underlying disorder, monitor ventilatory status and implement mechanical ventilation if needed

Respiratory alkalosis: pH high, pCO2 low

Diagnostic Clues: hyperventilation, light-headedness, paresthesias of lips and limbs, tetany, syncope, seizures

Expected correction factors:  

Acute respiratory alkalosis: decrease in HCO3 = 0.2* pCO2 

Chronic respiratory alkalosis: decrease in HCO3 = 0.4* pCO2

Causes: anxiety, brainstem tumors, drugs, infection, sepsis, pulmonary embolus, pneumonia, interstitial lung disease

Treatment:  correct underlying disorder, monitor ventilatory status and implement mechanical ventilation if needed


Electrolyte Abnomalities

Hypokalemia

Diagnostic Clues: weakness, fatigue, muscle cramps, constipation, arrythmias; EKG may show flattened T-waves, U-waves, and ST-depression

Causes: diuretics, vomiting, NG drainage, Mg2+ depletion, renal tubular acidosis

Treatment:  replace potassium, treat underlying disorder; evaluate for hypomagnesemia and replace as needed – these often occur together

Hyperkalemia

Diagnostic Clues: nausea, vomiting, weakness, palpitations, paresthesias; EKG may show peaked T-waves, increased P-R interval, widened QRS, “sine wave”

Causes: acidemic states (e.g., DKA, uremia, type 4 RTA, etc), dig intoxication, crush injuries, renal failure, many drugs (know the common ones:  ACE inhibitors, ARB’s, etc.)

Treatment:  calcium gluconate, bicarbonate, insulin & glucose, kayexelate, lasix, albuterol  if significant elevation of potassium not responding to above therapies  dialysis

Hypocalcemia

Diagnostic Clues:  abdominal cramps, tetany, perioral paresthesias, positive Chvostek’s sign (facial spasm in response to tapping over facial nerve) or Trousseau’s sign (carpal spasm induced by inflation of blood pressure cuff); prolonged QT interval

Causes:  acute pancreatitis, vitamin D deficiency, malnutrition, hypoparathyroidism

Treatment:  treat underlying disorder and replace calcium

Hypercalcemia

Diagnostic Clues:  “bones, stones, groans, and psychiatric overtones”  or in other words fractures, kidney stones, constipation, altered mental status, weakness, shortened QT interval

Causes:  malignancy (multiple myeloma, squamous cell carcinoma) and hyperparathyroidism

Treatment:  IV fluids (NS) then furosemide to eliminate calcium; bisphosphonate

Hypomagnesemia

Diagnostic Clues:  GI complaints, muscle weakness, prolonged QT interval

Causes:  diuretics, cisplatin, malnutrition/malabsorbtion, vomiting, pancreatitis, DKA, EtOH

Treatment:  treat underlying cause and replace magnesium

Hypermagnesemia

Diagnostic Clues:  pulmonary edema, decreased DTRs, tetany

Causes:  iatrogenic, Addison’s disease, dehydration, DKA, hypothyroidism, multiple myeloma, renal failure

Treatment:  IVF and diuretics, identify and treat underlying cause

Hyponatremia

Diagnostic Clues:  confusion, nausea; if chronic may be asymptomatic; if severe may result in seizures or brain stem herniation

Causes:  renal failure, nephritic syndrome, renal failure, drugs, psychogenic polydipsia, SIADH, CHF, cirrhosis, diuretics, vomiting, dehydration

Treatment:  if hypervolemic or euvolemic  water restriction; if hypovolemic  replete with normal saline; chronic hyponatremia should be corrected slowly to prevent central pontine myelinolysis

Hypernatremia – water loss is most common cause (along with lack of access to free water—e.g., impaired thirst mechanism)

Diagnostic Clues:  pt may complain of being thirsty, may have mental status changes, pulmonary or peripheral edema

Causes:  diabetes insipidus, hypertonic sodium gains, hyperaldosteronemia, hypotonic fluid losses

Treatment:  treat the underlying cause and then gradually correct sodium level to prevent neurologic damage

Hypophosphatemia

Diagnostic clues: weakness, muscle pain, bone pain, respiratory distress, neurologic dysfunction

Causes: chronic alcoholism, malnutrition, medications

Refeeding syndrome

Occurs in patients receiving parenteral, enteral, or oral feedings after period of sustained malnutrition or starvation

Triad of hypophosphatemia, hypokalemia, and hypomagnesemia (introduction of carbohydratesinsulin secretionthese electrolytes move intracellularly)

Uncommon but potentially fatal

Treatment: treat underlying cause, oral phosphate replacement therapy usually adequate

Hyperphosphatemia

Diagnostic clues: usually asymptomatic, but may have symptoms of concurrent hyocalcemia

Causes: almost exclusively in patients with kidney disease/failure 

Labs: follow calcium and renal function

Treatment: address underlying issues, calcium carbonate or calcium acetate

Cannot dialyze!