Postrenal failure: Caused by urinary outflow obstructions in one or both ureters, the bladder neck, the urethra, or the prostate.
To ensure the patient's safety, order an ECG (may show a short QT interval).
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The pituitary does not make ADH.
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Check calcium, phosphate, albumin, ionized calcium, and alkaline phosphatase.
When serum sodium is low or rapidly decreasing, hyponatremia may lead to cerebral edema that may result in seizures, status epilepticus, coma, or even death.
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Examination should include checking BP, daily weights, and assessment of volume status.
Next, follow the mnemonic C BIG K Drop.
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Effects of hyperkalemia as seen on ECG.
Also consider vitamin D levels, SPEP, TSH, and imaging.
Identify and treat the underlying cause.
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Tx: Replace with calcium carbonate orally or with IV calcium gluconate.
Consider ordering a CXR.
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What are the next steps in diagnosis?
Start by administering calcium to stabilize the heart.
The kidneys are unresponsive to ADH.
GI absorption (as found in hypoparathyroidism, pseudohypoparathyroidism, vitamin D deficiency, malabsorption, renal failure, critically ill patients, and hypomagnesemia), acute pancreatitis, rhabdomyolysis, tumor lysis, and diuretics.
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What do you do next?
Evaluate the patient for urinary retention, as this is likely the cause of his renal failure.
You call the laboratory, and they state that the specimen was not hemolyzed.
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ARF but should prompt one to test for it.
Intrinsic failure: Can be vascular, glomerular, tubular (most common), or interstitial.
Posm ratio to help determine the cause.
She is feeling well.
Envision a salty desert.
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Causes of Acute Renal Failure.
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What should you do next?
Alkalosis is most commonly associated with Proteus UTIs but may also be seen with some strains of Klebsiella, Pseudomonas, Providencia, and Staphylococcus.
CHF before giving the bolus!
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Hemodialysis is a last resort.
Acidosis with nephrolithiasis suggests uric acid or cystine stones.
Consider in patients with pancreatitis, refractory peptic ulcer disease, a personal or family history of kidney stones, or bone pain.
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D5W, or oral water depending on the patient's volume status.
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Do not give patients with SIADH NS, as this can paradoxically worsen the hyponatremia.
Get an ECG, as this may show serious signs of hyperkalemia.
The man has a past medical history of smoking and CAD.
Bladder neck: Anticholinergics, tumor.
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Usually indicates that the kidneys are wasting potassium.
Pyelonephritis or interstitial nephritis.
Acute interstitial nephritis yields a UA with eosinophils, WBCs, and WBC casts.
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ATN, acute interstitial nephritis, vasculitis, or anything causing renal ischemia.
Often asymptomatic, but may present with confusion, lethargy, muscle cramps, and nausea.
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Check plasma and urine osmolalities and sodium.
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Euvolemic hyponatremia: If the patient is symptomatic, give hypertonic NS with furosemide.
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Other findings are specific to the etiology of the renal failure.
Patients can present in fluid overload from urinary retention.
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Usually indicates a nonrenal source of hypokalemia.
Order a repeat blood draw unless suspicion is high.
May present with fatigue, muscle weakness or cramps, ileus, hyporeflexia, paresthesias, and flaccid paralysis if severe.
Severe or symptomatic hyperkalemia, hyperkalemia refractory to the above management, or patients on chronic hemodialysis may require acute hemodialysis.
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Restrict dietary potassium and discontinue any medications that may be contributing to the hyperkalemia.
Given this patient's worsening cough, you might also consider a CXR, as this may be relevant in the setting of SIADH.
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Finally, you can give Kayexalate and furosemide to dispose of the excess potassium.
Urine potassium levels can help determine the etiology of the hyperkalemia.
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You may be able to bump hyponatremia to the bottom of your problem list, but central pontine myelinolysis will go to spot number one!
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Note that overly rapid correction may result in central pontine myelinolysis (flaccid paralysis, dysarthria, dysphagia, and gait abnormalities).
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Uosm should not respond to DDAVP challenge.
Causes include excessive hydration with hypertonic fluids, dysfunction of central regulation, and mineralocorticoid excess (consider if the patient has hypokalemia and hypertension).
WBCs is always abnormal except when the sample is contaminated (eg, with epithelial cells).
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If the patient has a large postvoid residual, he should keep his Foley in place and be referred to urology.
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PTHrP secretion from cancer cells (often squamous cell carcinoma) can cause a paraneoplastic hypercalcemia.
DM, is in the hospital receiving IV antibiotics for pyelonephritis.
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