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|

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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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