Nephrology - Stanford University
Causes
• Prerenal: decreased effective arterial volume (hypovolemia, CHF, sepsis), ACE-I, NSAIDs
• Acute tubular necrosis (ATN): progression of prerenal state, drugs (aminoglycosides, ampho, cisplatin), myo- or hemoglobinuria, multiple myeloma. Sediment: muddy brown granular casts
• Contrast-induced acute renal failure: peaks in 3-5 days, resolves in 7-10 days
– If high-risk: pre- and post- hydration and N-acetylcysteine 600 mg po bid on day prior to and day of contrast with iv hydration
• Acute interstitial nephritis (AIN): drugs (antibiotics, NSAIDs) or infection; sediment: WBC casts, WBCs, RBCs; may be associated with fever, rash, eosinophilia, and eosinophiluria
• Vascular: RAS (+ ACE-I), thrombosis, hypertensive crisis, scleroderma, cholesterol emboli, HUS/TTP, preeclampsia
• Acute glomerulonephritis: sediment may show dysmorphic RBCs and RBC casts
• Post-renal: obstruction (malignancy, BPH, bilateral stones), neurogenic bladder, anticholinergics
Workup
• Degree of and type of workup varies depending on history
• Examine urine sediment
• Determine if patient is oliguric/anuric (output 18), tumor lysis syndrome (in settings of very high uric acid)
• Intoxications. Lithium, salicylates, theophylline, alcohols
• Overload (volume)
• Uremia (with complications, e.g. pericarditis)
Hemodialysis (HD)
• Principle. Blood flows along one side of a semipermeable membrane, dialysate along the other. Fluid removal occurs via pressure gradient. Solute removal occurs via concentration gradient, and in a manner inversely proportional to molecular size (effective at removing potassium, urea, creatinine but not very effective for removing PO4).
• Access. Double-lumen central catheter (tunneled or temporary), AV fistula, or AV graft
• Contraindications. Hemodynamic instability (see CVVH), arrhythmias, bleeding
• Complications. Hypotension (from ultrafiltration, medication, temperature of dialysate, bleeding, infection, arrhythmia, ischemia), arrhythmias, HIT, access complications
Continuous veno-venous hemofiltration (CVVH)
• Indications. Patients who are hemodynamically unstable and who are not likely to tolerate the large fluid shifts associated with HD
• Principle. Blood flows along one side of a highly permeable membrane and fluids and solutes pass by convection. Filtrate is discarded and fluid with plasma-like solute concentrations is infused. Fluid balance is precisely controlled by adjustment of the quantity of replacement fluid infused.
• Anticoagulation by citrate v. heparin and bicarbonate. Citrate achieves regional anticoagulation by calcium chelation (metabolized in liver); contraindication is liver failure. Need to watch calcium levels and citrate toxicity (suggested by rising total calcium, falling ionized calcium, rising anion gap).
• Complications. Hypotension, hypophosphatemia, hypocalcemia, access complications
Peritoneal dialysis
• Principle. Gravity assisted infusion into peritoneum; control H2O and Na balance by adjusting the glucose concentration in the fluid; very long dwell times pull out less fluid as the glucose equilibrates
• Access. Catheter placed by transplant surgery generally.
• Contraindications. Recent abdominal surgery, infection, ileus
• Orders: PD fluid: 1.5%, or 2.5 %, or 4.25% dextrose (higher dextrose removes more fluid)
• Typical prescription. Volume 2 L, dwell time 6 hours, dextrose 1.5% for a total of 4 exchanges in 24 hour period. Prescription written generally by peritoneal dialysis nurse (PD unit 617-720-1317). PD nurse on call 24/7 for any issues.
• Complications
– Infection: fairly common. Can occur at exit site, tunnel, and/or peritoneum. Catheter removal may be necessary especially if fungal infection. Diagnose by finding >100 WBC with >50% PMN in fluid. 50-60% infections are GPC, 15-20% GNR, remainder are fungal or no identifiable organism. Can treat with either intravenous or peritoneal antibiotics.
– Hyperglycemia: exacerbated by inflammation, long dwell time, and higher dextrose concentrations. Treat by adding insulin sc
– Clots: add heparin in first few infusions (but involve renal)
General considerations
• Determine if patient is alkalemic (pH>7.44) or acidemic (pH40 ( respiratory acidosis
– HCO3 20 and euvolemia suggests saline-resistant metabolic alkalosis:
– if hypertensive: hyperaldosteronism, Cushing’s syndrome, licorice ingestion, Liddle’s
– if normotensive: extreme hypokalemia, exogenous alkali, Bartter’s, Gitelman’s
Respiratory acidosis
• CNS depression, especially from medications
• Airway disease: COPD, asthma, upper airway abnormalities
• Neuromuscular disease
• Parenchymal lung disease: pneumonia, pulmonary edema, restrictive lung disease
• Thoracic cage abnormalities: pneumothorax, kyphoscoliosis
Respiratory alkalosis
• Any cause of hypoxia causing increased respiratory drive (e.g. pneumonia, pulmonary embolism, pulmonary edema)
• Pain, anxiety
• Salicylates
• Pregnancy/progesterone
• Sepsis
• Liver failure
• Primary CNS disorder
EKG changes in hyperkalemia
• Patterns best seen in leads V4-5
• Correct diagnosis can usually be made when K > 6.7.
|K |EKG changes |
|> 5.5 |peaking in T waves |
|> 6.5 |QRS widening |
|> 7 |P wave amplitude decreases, duration of P wave increases, prolongation of PR interval |
|> 8 |P wave disappears, auricular standstill |
|> 10 |ventricular rhythm may become irregular and may simulate atrial fibrillation |
|> 12-14 |asystole or ventricular fibrillation |
General considerations
• Interpatient variability in effects of hyperkalemia, time course of hyperkalemia (e.g., end stage renal disease vs. acute tissue break down)
• K > 7, EKG changes, changes in muscle strength generally warrant immediate treatment
|Therapy |Dose |Onset of effect |Duration of |Comments |
| | | |effect | |
|Calcium |10 mL (1 amp) of 10% calcium gluconate or calcium|1-3 min |30-60 min |Stabilizes cardiac membrane |
| |chloride solution infused over 2-3 min | | |Caution in patients taking digoxin as |
| | | | |hypercalcemia can induce digitalis |
| | | | |toxicity |
|Sodium bicarbonate |1 mEq/kg iv bolus (1 amp of sodium bicarb ~45 |5-10 min |1-2 hours |K lowering most prominent in metabolic |
| |mEq) | | |acidosis |
|Insulin and glucose |10 U iv plus D50 1-2 amps (note more than 1 amp |30 min |4-6 hours |Enhances Na-K-ATPase pump in skeletal |
| |may be needed to prevent hypoglycemia) | | |muscle |
| | | | |Causes 0.5-1.5 mEq/L fall in K |
|Albuterol, nebulized |10-20 mg nebulized over 15 min |15 min |15-90 min |Drives potassium into cells by increasing|
| | | | |Na-K-ATPase activity |
| | | | |Lowers K by 0.5-1 |
|Kayexalate (Na |15-50 g po or pr, plus sorbitol |1-2 hours |4-6 hours |Binds K in gut and releases Na |
|polystyrene sulfonate) | | | | |
|Diuresis |Furosemide 40-80 mg iv | | | |
|Dialysis | | | |Consider dialysis when conservative |
| | | | |measures fail, if hyperkalemia is severe,|
| | | | |or if ongoing hyperkalemia a likely issue|
-----------------------
Glomerular diseases
1. Anti-GBM disease (e.g. Goodpasture’s)
2. ANCA-associated
– Wegener’s
– Polyarteritis nodosa
3. Immune-complex associated
– SLE
– MPGN
– Cryoglobulinemia
– Etc.
Ishir Bhan, M.D.
Respiratory acidosis
acute, (pH 0.08 for (10 mm Hg pCO2
chronic, (pH 0.03 for (10 mm Hg pCO2
Respiratory alkalosis
chronic, (pH 0.02 for (10 mm Hg pCO2
Ishir Bhan, M.D.
Remember to correct for hyperglycemia. (Hyperlipidemia and paraproteinemia are no longer a problem with Na measurement at MGH given newer lab technique due to electrode.)
Hyponatremia
If hyponatremia is severe, hypertonic saline may be needed.
Caution when correcting hyponatremia too rapidly because of possible pontine osmotic demyelination.
In asymptomatic patients, recommended average correction of 0.5 mEq/L per hour.
Hypernatremia
Sodium + H2O restriction
May need diuretic
Treat underlying condition
Free H2O restriction
Treat underlying condition
Isotonic saline
Mineralocorticoid prn
UNa 20
UNa >20
Low circ volume
CHF
Cirrhosis
Nephrotic synd.
Normal circ volume
Renal failure
SIADH
Glucocorticoid deficiency
Thyroid dysfunction
Reset osmostat
Extrarenal loss Vomiting
Diarrhea
Third spacing
Renal loss
Osmotic diuresis
Diuretics
Mineralocort deficiency
Na-losing nephropathy
UNa 20
Extracellular volume excess
Extracellular volume normal
(mild excess)
Extracellular volume deficit
Diuretics + H2O
Free H2O replacement
Volume replacement with normal saline, free H2O replacement with hypotonic saline
Hypertonic HD
NaHCO3 treatment
Extrarenal loss
Insensible losses
Renal loss
Central DI
Nephrogenic DI
Extrarenal loss
Perspiration
Diarrhea
Renal loss
Osmotic diuresis
UNa 20
UNa >20
UNa variable
Na excess
Na >H2O
H2O stores depleted
Na stores relatively normal
Na stores depleted
H2O depleted >Na
[pic]
No specific disorder
Magnesium depletion
Cisplatin
Recovery from ARF
Post-op diuresis
Metabolic alkalosis
Vomiting
Nasogastric suction
Diuretics
Increased mineralocorticoid
Bartter’s
Metabolic acidosis
Type 1 RTA
Type 2 RTA
Carbonic anhydrase inhibitors
Uretero-sigmoidostomy
• During hypokalemia, the expected TTKG is 10. A lower value suggests that that K+ secretion is inappropriately suppressed (e.g., in hypoaldosteronism).
Renal loss (high TTKG)
Extrarenal loss
(low TTKG)
Diarrhea
Laxative abuse
Villous adenoma
Sweat losses
Inadequate intake
Redistribution
Insulin
Alkalemia
Beta2 agonist
Theophylline toxicity
Familial hypokalemic periodic paralysis
Spurious
WBC >100,000 (if left at room temperature, WBC may take up K)
Hypokalemia
Hyperkalemia
Aldosterone unresponsiveness
SLE
Amyloid
Obstructive uropathy
Renal transplant
Aldosterone insufficiency
Addison’s
Hyporenin-hypolado
Normal GFR
Low GFR (10-20% of nl)
Impaired K excretion
Renal failure
Aldosterone insufficiency
Other (drugs)
K sparing diuretics
ACE inhibitors
Pseudohyperkalemia
Hemolysis
Plts >1,000,000
WBC >200,000
Familial pseudohyperkalemia
Tourniquet-related
Sample drawn upstream from iv solution containing K
Redistribution
Acidosis
Hypertonic states
Digoxin overdose
Hyperkalemic periodic paralysis
Beta blocker
Usually in assoc with endogenous or exogenous potassium load
Reshma Kewalramani, M.D.
Reshma Kewalramani, M.D.
Andrew Yee, M.D.
Ishir Bhan, M.D.
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