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Nephrology

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Erythrocyte casts

  • Glomerular disease

Leukocyte casts

  • Inflammation/infection of parenchyma

Muddy brown casts

  • ATN

Broad casts

  • CKD

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When is Winter’s formula used?

  • When you have a metabolic acidosis and want to check for respiratory compensation

  • pCO2 = 1.5(bicarb) + 8 +/- 2

  • Measured CO2 = predicted CO2 -> pure metabolic acidosis

  • Measured CO2 > predicted CO2 -> metabolic acidosis and respiratory acidosis

  • Measured CO2 < predicted CO2 -> metabolic acidosis and respiratory alkalosis

  • Delta/delta <0.5-1 = consider concurrent non gapped acidosis 

  • Delta/delta >2 = consider concurrent metabolic alkalosis


 

In acute respiratory acidosis how much should bicarb be expected to increase? 

  • 1mEq/L for every 10 mm Hgb increase in CO2

 

In chronic respiratory acidosis how much should bicarb be expected to increase? 

  • 3.5 for every 10 increase in CO2

 

In metabolic alkalosis how much should CO2 be expected to increase? 

  • 0.7 for every 1 bicarb

 

What are the causes of a high anion-gap metabolic acidosis? 

  • Lactic acidosis

  • ketoacidosis (diabetic, alcoholic, starvation)

  • Toxins

  • AKI or CKD

 

What are the causes of a normal anion-gap metabolic acidosis?

  • GI bicarb losses (diarrhea)

  • Renal tubular acidosis

  • CKD

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What is renal tubular acidosis?

  • Kidneys do not remove acid properly from the blood into the urine

 

Define a Type 1 (hypokalemic distal) renal tubular acidosis:

  • Location: distal tubules

  • Pathophysiology: Inability to excrete acid in urine → basic urine, potassium-wasting

  • Causes: Sjogren syndrome, reflex and obstructive uropathy

  • Complications: calcium phosphate kidney stones

  • Treatment: potassium citrate

  • Urine anion gap: Yes

  • Urine pH: >6.0

  • Potassium: Hypokalemia

 

Define a Type 2 (proximal) renal tubular acidosis:

  • Location: proximal tubules

  • Pathophysiology: Inability to absorb bicarbonate → low bicarb levels → distal tubule fixes urine so urine can still be acidified

  • Causes: Myeloma, meds (ifosfamide, acetazolamide, tenofovir)

  • Complications: Fanconi syndrome, glycosuria, proteinuria

  • Treatment: alkali replacement, thiazide diuretics

  • Urine anion gap: No → ammonium and chloride are being excreted distally

  • Urine pH: <5.5

  • Potassium: Hypokalemia

 

Define a Type 4 (hyperkalemic distal) renal tubular acidosis:

  • Location: adrenal

  • Pathophysiology: Aldosterone deficiency or resistance → decrease in buffering capacity

  • Causes: Diabetic kidney disease, Addison disease, sickle cell

  • Treatment: correct underlying causes, thiazide/loop diuretics

  • Urine anion gap: Mild

  • Urine pH: <5.5

  • Potassium: Hyperkalemia

 

How is urine anion gap used to help determine etiology of RTA?

  • Urine anion gap= unmeasured cations (NH4+) - unmeasured anions = UNa +UK -UCl

  • Positive value (low NH4+): renal losses (RTA, carbonic anhydrase inhibition, adrenal insufficiency, normal saline infusion)

  • Negative value (high NH4+): GI losses (diarrhea, pancreatic fistula, ureterosigmoidostomy)

  • Caveat: Prox RTA has normal distal urine acidification and has a negative urine AG

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How is AKI/ARF define based on 2012 KDIGO Guidelines?

  • Rise in serum Cr > 0.3 within 48h or increase in >1.5 x baseline in 7 days

  • Urine volume <0.5cc/kg/h for >/= 6 hours

 

What is the typical BUN:Cr, urine osmolality, urine sodium, and FeNa in prerenal vs ATN?

  • Prerenal: >20:1, >500, <20, <1% (respectively)

  • ATN: 10:1, ~300, >40, >2%

 

In the setting of diuretic use what should be used instead of FeNa? 

  • FeUrea; <35% consistent with prerenal etiology

 

Eosinophilia/uria and rash should make you think of what two things? 

  • AIN and cholesterol emboli

 

Which cause of AKI is an ACE-i actually indicated in? 

 

Compare prerenal/intrarenal/postrenal AKI:

  • Prerenal - Caused by underperfusion of the kidney with a subsequent decrease in GFR

    • Due to intravascular volume depletion, decreased effective arterial circulation and renal vasoconstriction

  • Intrarenal - occurs from structural damage to the renal tubules, interstitium, glomerulus or vascular structures or from intratubular obstruction

    • Typical cause is acute tubular necrosis which is due to ischemia, nephrotoxins and/or sepsis

    • Other causes include acute interstitial nephritis, acute glomerulonephritis and intralobular obstruction

  • Postrenal - occurs from obstruction anywhere from the renal pelvis to the external urethral meatus

    • Should be suspected in patients with hx of BPH, diabetes, nephrolithiasis, pelvic malignancies, prior retroperitoneal radiation therapy, abdominal/pelvic surgeries or retroperitoneal adenopathy

 

Which type of azotemia is most often seen in the inpatient setting?

  • Prerenal and ATN

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What is CKD defined as?

  • Decreased kidney function or one or more markers of kidney damage for 3 or more months

 

Which interventions slow the progression of CKD? 

  • Glycemic control, blood pressure control, ACEs/ARBs, SGLT2s

 

The presence of what pathology in diabetes strongly suggests coexisting diabetic kidney disease? 

  • Retinopathy

 

Leading cause of death in patients with CKD? 

  • Cardiovascular disease

 

Common symptoms of uremia? 

  • Fatigue, nausea, loss of appetite, insomnia, difficulty concentrating, pruritus, dysgeusia

 

Worst side effects of azotemia (elevated BUN)? 

  • Acidosis, uremic pericarditis, platelet dysfunction, uremic frost

 

What does gadolinium put patients with CKD at risk for? 

  • Nephrogenic systemic fibrosis; greatest risk is in patients on dialysis

 

Role of statins in ESRD? 

 

What medications should you use in autosomal dominant polycystic kidney disease? 

  • ACE/ARB, but then tolvaptan has been shown to slow kidney function decline and should be added in pts with progressive disease

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What are the primary causes based on presentation of hematuria?

  • Transient- exercise-induced, trauma, menses

  • Concurrent pyuria/ dysuria- consider UTI or malignancy

  • Recent URI- consider infection-related GN, IgA, vasculitis, anti-GBM

  • Positive FHx- consider PKD, SCD

  • Bleeding from other sites- consider inherited/ acquired bleeding d/o, AC

  • Unilateral flank pain- consider ureteral calculus, renal malignancy, IgA nephropathy

 

Indications for urologic evaluation with CT urography and cystoscopy? 

 

How does erythrocyte morphology help to distinguish glomerular from extraglomerular hematuria? 

  • Glomerular diseases will have erythrocyte casts and dysmorphic erythrocytes however their absence does not rule it out

 

What is the work-up of glomerular bleeding?

  • If isolated hematuria → IgA nephropathy, thin BM dx, Alport’s

  • If nephritic syndrome suspected (new proteinuria, pyuria, HTN, edema, rise in Cr) → post-infectious GN, MPGN, ANCA vasulitis, Goodpasture’s, lupus nephritis

  • Work-up: anti-GBM, anti-DNase/ASO, ANA, ANCA, C3/C4, cryo, HBV/ HCV, HIV

  • Consider renal bx: glomerular bleeding plus risk factors for progressive disease

 

What are the urine findings in rhabdo? 

  • + blood on dipstick, negative erythrocytes on microscopy

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What is your first step when you see a low sodium on labs? 

  • Get an H&P! Determine red flags (confusion, seizures), new medications, nutritional status, fluid intake, alcohol intake

  • But also check serum osmolality 

 

What is the significance of serum osmolality?

  • Serum osmolality in true hyponatremia is <280 mOsm/kg

  • Sodium is the most significant contributor to osmoles in the osmolality equation

  • Rules out measured osms (hyperglycemia, elevated urea), unmeasured osms (from toxic alcohols - elevated osmolar gap), and pseudohyponatremia (paraproteins, elevated triglycerides)

  • For every 100 increase in glucose, sodium decreases by ~2

 

What is urine osmolarity?

  • Correlates with ADH activity

 

What does a low urine osmolarity tell you?

  • Low urine osm (<100-200) means urine is very dilute and ADH activity is low and points towards a hypotonic hyponatremia

  • Either increased in free water intake (psychogenic polydipsia) or decrease in solute intake (tea-and-toast) or both (beer potomania)

 

What does a high urine osmolarity tell you?

  • High urine osm (>200-300) means that urine is very concentrated and ADH activity is high

  • Does not tell you if ADH activity is appropriately or inappropriately high

 

What is urine sodium?

  • Correlates with RAAS activity

 

What does a low urine sodium tell you?

  • Low urine sodium (<20mEq/L) means RAAS is activated, responding to low effective arterial blood volume (EABV) = Appropriate

  • Body is trying to hold onto sodium (sodium-avid)

  • Appropriate ADH activation indicates low EABV from hypovolemia or sensed hypovolemia (CHF, cirrhosis)

 

What does a high urine sodium tell you?

 

What are common medications that can cause SIADH? 

  • Thiazides, SSRIs, TCAs, opioids, ecstasy

 

How do you treat hypovolemic hyponatremia?

  • Give volume and monitor response

  • If Na <120, then should give 3% saline and monitor response (monitor in ICU)

 

How do you treat SIADH?

  • Remove offending agent, if possible

  • Free water restrict

  • Can give tolvaptan (ADH antagonist) x 1 dose but is cost-prohibitive, limited to once a month due to potential liver toxicity

  • Can give 3% saline, if severe

  • No therapeutic benefit to give diuretics (higher likelihood of AKI and hypokalemia)

 

How quickly can you correct sodium?

  • If chronic (>48 hrs), goal is to increase by 4-6 mEq/L in 24-hour period, do not exceed 8 mEq/L given risk for osmotic demyelination syndrome

  • Most cases, you should assume chronic hyponatremia

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What are the three causes of hypernatremia?

  • Hypotonic losses via decreased water intake, diarrhea, sweating, osmotic diuresis

  • Hypertonic from administration of hypertonic saline, sodium bicarbonate, salt ingestion

  • Diabetes insipidus - Central (tumors) or Nephrogenic (drugs, ex. lithium)

 

What is the treatment of hypernatremia from hypertonic losses?

  • If there is hemodynamic compromise, give isotonic saline

  • Otherwise, administer water as 5% dextrose or 0.45% NSS (calculate total water deficit)

 

What is the treatment of diabetes insipidus?

  • Central = can give desmopressin (vasopressin analogue)

  • Nephrogenic = low-salt diet to decrease free water excretion, thiazide diuretics

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When to treat?

  • If over 6.0 or over 5.5 with EKG changes

 

Typical progression of EKG changes in hyperkalemia?

  • Peaking of T waves -> shortening of QT interval -> prolonged PR -> widening of QRS

 

Treatment of hyperkalemia?

  • Stabilize cardiac membrane = Calcium gluconate

  • Buy yourself time = Insulin/Dextrose, B-agonists

  • Actually treat = Lasix, Lokelma, Dialysis

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How is hypertension defined?

  • >130/80 mmHg, checked 2 or more times on 2 or more occasions

 

What are the main classes of anti-HTN agents?

  • Calcium-channel blockers (amlodipine, nifedipine, diltiazem (Non-DHP)

  • ACE-i/ARB

  • Beta-blockers

  • Aldosterone receptor antagonists (spironolactone, eplerenone)

  • Loop diuretics (furosemide, torsemide, bumetanide)

  • Thiazide diuretics (hydrochlorothiazide, chlorthalidone)

  • Vasodilators (hydralazine, minoxidil)

  • A-blockers (doxazosin, prazosin)

  • Central sympathetic agonists (clonidine)

 

When should you use multiple anti-HTN agents?

  • If average BP is >150/90 (20/10 mmHg above goal)

 

How should you treat hypertension in a patient with diabetes and albuminuria?

  • ACE-i/ARB

 

How should you treat hypertension in a patient with CHF? (Not HFrEF)

  • Thiazide diuretic >> ACE-i >> MRAs (spironolactone) >> CCBs

 

What is hypertensive emergency?

  • Elevated BP (usually >180/120 but no specific threshold) with end-organ damage = stroke, encephalopathy, AKI, MI, dissection, acute CHF

 

What are the treatment goals with hypertensive emergency?

  • Initial lowering should be 10-20% in the first hour and by a further 5-15% over the next 23 hours (exceptions include acute ischemic stroke, acute aortic dissection, ICH, all of which have more specific guidelines in BP lowering)

 

Which IV medications are used in the treatment of hypertensive emergency?

  • Nicardipine (most common)

  • Nitroglycerin (use with flash pulmonary edema or ACS)

  • Labetalol (don’t use in asthma, COPD, acute CHF, or bradycardia)

  • Nitroprusside (risk of tachyphylaxis, cyanide toxicity)

 

What medications should you reach for antihypertensives in a pregnant patient? 

  • Labetalol, nifedipine, methyldopa

 

What are the causes of secondary hypertension?

  • AKI or CKD, renal artery stenosis, primary hyperaldosteronism, pheochromocytoma and sleep apena

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What is defined as resistant hypertenion?

  • Blood pressure that remains above 140/90 mmHg despite use of three antihypertensive medications of different classes at the best tolerated doses, one of which must be a diuretic

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What is the best initial study in the evaluation of nephrolithiasis? 

  • Ultrasound! This is a newer recommendation. However, your decision should also be based on the situation as ultrasound is less sensitive at detecting small stones, but is more cost-effective and does not expose patients to radiation.

  • Ultrasound is favored when there is high clinical suspicion for stones, for younger patients, and patients with a normal BMI. Non-contrast helical CT remains the best study for more complicated presentations of nephrolithiasis or if ultrasound is nondiagnostic but clinical suspicion remains high

  • https://pubmed.ncbi.nlm.nih.gov/27578040/#&gid=article-figures&pid=figure-1-uid-0

 

Which size stones typically pass on their own? 

  • <5mm

 

Which size stones typically require invasive measures? 

  • >10 mm

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What is the most common cause of nephrotic syndrome in kids? 

  • Minimal change

 

In whom and how does membranous nephropathy present? 

  • Middle-aged adults or elderly adults with malignancy

  • usually slow presentation and may present with AKI due to renal vein thrombosis; associated with Hep B/C, SLE, NSAIDs, certain cancers

 

What antibody is membranous nephropathy associated with?

  • Anti-phospholipase receptor A2 antibodies

 

What disease is the collapsing variety of FSGS associated with? 

  • HIV

 

What are complications of nephrotic syndrome?

  • Renal vein thrombosis

 

What is the most serious extrarenal complication of ADPKD? 

  • Ruptured intracranial cerebral aneurysm

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