Nephrology UWorld

Acute urinary retention

- Agitation - Tachycardia - Suprapubic tenderness - Can cause constipation First generation antihistamines (diphenhydramine, chlorpheniramine, hydroxyzine) also have significant anticholinergic effects (at muscarinic receptors of the parasympathetic nervous system), TCAs - Impaired detrusor muscle contraction - Impaired internal sphincter relaxation Risk: - Male, > 80 - BPH - Neurologic disease - Surgery (abd surgery, pelvic surgery, joint arthroplasty) - Opioids, anticholinergics Dx: bladder US > 300 mL of urine Tx: Foley catheter, UA (r/o UTI) - Foley may be both therapeutic and diagnostic if pt is fat as ****

Microscopic polyangiitis

- Constitutional symptoms of fever & malaise - Abdominal pain - Hematuria w/ active urine sediment - Purpura ANCAs in serology w/ normal serum complement

Granulomatosis with angiitis

- Ear, nose, throat, and pulmonary manifestations - Renal involvement and nephritic syndrome - C3 levels normal (complement not affected)

Benign prostatic hyperplasia (BPH)

- Extrinsic compression of the urethra - Urinary urgency - Difficulty initiating and maintaining urine stream - Incomplete bladder emptying

Systemic lupus erethematosus (SLE)

- Gradual symptom onset - Malar or discoid rash - Joint, renal, serosal, or neurologic involvement - Photosensitive skin - Glomerulonephritis (renal failure with erythrocyte casts, proteinuria, HTN) - Nephrotic syndrome - RPGN - Pulmonary renal syndrome Lab: - Anemia, leukopenia, thrombocytopenia - ANA, anti-dsDNA, anti-Smith - Low complement levels (C3-C4), increased immune complexes

RBC transfusion thresholds

- Hb < 7 (generally indicated) - Hb 7-8 (cardiac surgery, oncology pts in tx, heart failure) - Hb 8-10 (symptomatic anemia, ongoing bleeding, ACS, noncardiac surgery) - Hb > 10 not generally indicated

Gastrointestinal electrolyte losses (vomiting)

- Hypochloremia - Hypokalemia - Elevated bicarbonate GI fluid is rich in hydrogen chloride and potassium chloride. Loss of hydrogen ions increases concentration of bicarb. Volume contraction caused by vomiting leads to activation of RAAS, which stimulates bicarb reabsorption. (alkalosis) Loss of potassium is also facilitated by alkalosis, which causes an intracellular shift of potassium to secrete hydrogen ions. Also by increased renal excretion of K and H+ due to aldosterone. (alkalosis and hypokalemia) Metabolic alkalosis pH > 7.4

Loop diuretics

- Hypokalemia - Metabolic alkalosis - Prerenal AKI Fxn by inhibiting the Na-K-2Cl carrier in loop of Henle, which results in increased loss of sodium and potassium in the urine. Also results in volume contraction and increased aldosterone levels, further promoting secretion of hydrogen ions in the urine.

Diuretic abuse

- Hyponatremia - Hypokalemia - Hypochloremia (diuresis & contraction alkalosis) - Increased urinary sodium - Increased urinary potassium - Hypovolemia - Orthostatic hypotension - Weight loss

Prevention of recurrent nephrolithiasis

- Increase fluids (produce > 2L urine/day) - Reduce sodium (<100 mEq/day) - Reduce protein - Normal calcium intake - Increase citrate (fruits and vegetables) - Reduced oxalate diet (if oxalate stones) w/ dark roughage, vitamin C - Thiazide diuretics - Urine alkalinization (potassium citrate/bicarbonate salt) - Allopurinol (for hyperuricosuria-related stones) Note: mild volume depletion caused by thiazide diuretics leads to compensatory rise in reabsorption of sodium and water with resulting increased passive reabsorption of calcium. May also function directly to increase calcium reabsorption from the tubule

Membranoproliferative glomerulonephritis (type II)

- Nephrotic range proteinuria - Hematuria - Dense intramembranous deposits that stain for C3 - IgG antibodies (C3 nephritic factor) directed against C3 convertase of the alternative complement pathway - These antibodies reacting with C3 convertase lead to persistent complement activation and kidney damage

Mixed cryoglobulinemia

- Palpable purpura - Proteinuria - Hematuria (glomerulonephritis) - Arthralgias - Hepatosplenomegaly - Hypocomplementemia - Peripheral neuropathy Many pts have underlying HCV infection Dx: demonstration of circulating cryoglobulins

Nephrotic syndrome

- Proteinuria (> 3-3.5 g/day) - Hypoalbuminemia - Edema - HLD - Hyercoagulation (AT3 loss, loss of protein C + S) Minimal change, membranous glomerulopathy, mesangial proliferative glomerulonephritis, membranoproliferative glomerulonephritis, FSGS Complications: - Renal vein thrombosis, PE - Protein malnutrition - Iron-resistant microcytic hypochromic anemia (loss of transferrin) - Vit D deficiency (due to increased urinary excretion of cholecalciferol-binding protein) - Decreased thyroxin levels (due to loss of thyroxine-binding globulin) - Increased infection risk

Obstructive urolithiasis (ureteral stone)

- Severe lower abdominal pain radiating to groin - Vomiting - Unremarkable findings on abdominal exam Acute obstruction at UVJ produces severe flank pain that radiates to perineum, penis, scrotum, or inner thigh. Pts often unable to sit still. Evaluation: - US (preferred in high suspicion pts and pregnancy) - Noncontrast spiral CT abdomen pelvis

Malignant cystic mass

- Thick irregular wall - Multilocular - Multiple septae, occasionally thick and calcified - Heterogenous content (solid and cystic) - Presence of contrast enhancement on CT/MRI - Pain, hematuria, HTN - F/u imaging and urological evaluation

Simple renal cyst

- Thin, smooth, regular wall - Unilocular - No septae - Homogenous content - Absence of contrast enhancement on CT/MRI - Usually asymptomatic - No f/u needed

Lower urinary tract symptoms (LUTS)

- Urinary urgency - Hesitancy - Nocturia - Weak urinary stream Evaluation: - Urinalysis (to exclude infection and hematuria) - Serum PSA (to assess for prostate cancer) - If acutely elevated Cr, obtain renal US (to assess for hydronephrosis/obstruction)

Indications for urgent dialysis

AEIOU: - Acidosis (metabolic acidosis pH < 7.1 refractory to medical therapy) - Electrolyte abnormalities (symptomatic hyperkalemia w/ ECG changes or ventricular arrhythmias or K > 6.5 refractory to medical therapy) - Ingestion (methanol, ethylene glycol, salicylate, Li, valproate, carbamazepine) - Overload (volume overload refractory to diuretics) - Uremia (symptomatic--encephalopathy, pericarditis, bleeding)

Anion gap

AG = Na - (Cl + HCO3)

Calcium oxalate stone

75-90% of kidney stones are composed of calcium oxalate (envelope shaped) Small bowel disease, surgical resction, or chronic diarrhea can lead to malabsoprtion of fatty acids and bile salts. Predisposes to the formation of calcium oxalate stones because fat malabsorption leads to the increased absorption of oxalic acid since the unabsorbed fatty acids chelate calcium, making oxalic acid free for absorption). Increased Na intake enhances calcium excretion (hypercalciuria). Low Na intake promotes Na and Ca reabsorption through its effect on the medullary concentration gradient.

Normal AG metabolic acidosis

AG = Na - (Cl + bicarb) normal = 10-14 - Diarrhea - Fistulas - Carbonic anhydrase inhibitors - Renal tubular acidosis - AKI (impaired H excretion, ammonia generation, or bicarb reabsorption) - Ureteral diversion - Iatrogenic

Cysteine stones

Formed when there is increased excretion of cysteine, which is an inborn error of metabolism

Anion gap metabolic acidosis

AG = Na - (Cl + bicarb) normal = 10-14 MUDPILES: - Methanol - Uremia (AKI) - DKA - Propylene glycol/Paraldehyde - Isoniazid/Iron - Lactic acidosis - Ethylene glycol - Salicylates

Anti-GBM disease (Goodpasture)

Anti-GBM antibodies against collagen IV damaging glomerular and alveolar lining. Manifests as either renal (RPGN) or alveolar hemorrhage (pulmonary renal syndrome--Goodpasture)

AA amyloidosis

Associated conditions: - Chronic inflammatory conditions (rheumatoid arthritis, IBD) - Chronic infections (osteomyelitis, TB) Composition of amyloid: - Abnormally folded proteins (beta-2 microglobulin, apolipoprotein, transthyretin) Can p/w nephrotic syndrome: - Renal Bx shows amyloid deposits that stain with Congo red and demonstrate apple-green birefringence under polarized light - Deposits found in glomerular BM, blood vessels, and interstitium of kidneys

AL amyloidosis

Associated conditions: - Multiple myeloma - Waldensrom macroglobulinemia Composition of amyloid: - Light chains (lambda) Can p/w nephrotic syndrome: - Renal Bx shows amyloid deposits that stain with Congo red and demonstrate apple-green birefringence under polarized light - Deposits found in glomerular BM, blood vessels, and interstitium of kidneys

Complicated cystitis

Associated with DM, pregnancy, renal failure, urinary tract obstruction, indwelling catheter, urinary procedure (cystoscopy), immunosuppression, and hospital acquired - Fluoroquinolones (5-14d), extended-spectrum abx (ampicillin/gentamicin) for more severe cases - Obtain sample for UCx prior to initiating therapy and adjust abx as needed Note: no fluoroquinolones in pregnancy. Consider cefpodoxime, cephalexin, augmentin, fosfomycin

Hyponatremia symptoms

Asymptomatic: 130-135 mEq/L Mild: 120-130 (lethargy, forgetfulness) Severe: < 120 (profound confusion, seizures, coma) - Increased risk of cerebral edema and herniation

Hypovolemic hyponatremia

Attempt to restore euvolemia at the risk of developing hypotonicity. - High renin - High ADH - High aldosterone - Low urine sodium Solute and water loss: Decreased renal perfusion --> activation of RAS --> Angiotensin II --> increased ADH, thirst, aldosterone --> Increased water absorption, intake, and sodium reabsorption --> lose solute faster than reabsorption so decreased total serum Na Hypotension --> baroreceptors --> increased ADH --> increased water absorption --> decreased serum Na Hypovolemia --> left atrial stretch receptor stimulation --> increased ADH --> increased water reabsorption --> decreased serum Na

Diabetic autonomic neuropathy

Cardiovascular: - Tachycardia, impaired exercise tolerance - Postural hypotenison Peripheral nerves: - Dry skin, pruritis, callus formation - Foot ulcers and poor wound healing - Charcot arthropathy (increased fracture risk) GI: - Gastroparesis with delayed gastric emptying - Esophageal dysmotility with possible dyspepsia - Intestinal involvement with possible diarrhea, constipation, or fecal incontinence GU: - Erectile dysfunction and retrograde ejaculation in men, decreased libido & dyspareunia in women - Decreased ability to sense full bladder leading to incomplete emptying and decreased urination - Eventual recurrent UTIs and/or overflow incontinence (dribbling, poor stream)

Acute interstitial nephritis

Causes: drugs (penicillins, TMP-SMX, cephalosporins, NSAIDs) - Maculopapular rash - Fever - New drug exposure - Arthralgias UA: AKI, pyuria, hematuria, WBC casts, eosinophilia, urinary eosinophils Renal biopsy: inflammatory infiltrate, edema Tx: d/c offending drug - Systemic glucocorticoids

Acute tubular necrosis

Characterized by acute azotemia following a hypotensive of nephrotoxic injury. Results in acute renal failure - Dark, cola-colored urine - Muddy brown casts

Thiazide adverse effects

Chlorthalidone, HCTZ - Impair insulin release from pancreas and glucose utilization in peripheral tissues (thiazide-induced glucose intolerance) --> hyperglycemia - More commonly seen in pts with diabetes and metabolic syndrome (HTN, dyslipidemia, abdominal obesity) - Increase LDL and TGs - Hyponaremia - Hypokalemia - Hypomagnesemia - Hypercalcemia - Can also decrease renal uric acid excretion, and hyperuricemia predisposes to gout

Workup of AG metabolic acidosis

Clinical clues... Drug ingestion: - Salicylates (early respiratory alkalosis) - Isoniazid - Iron Hypoperfusion: - Increased serum lactate --> lactic acidosis Renal failure - Elevated BUN --> uremia Hyperglycemia - Urine & serum ketones --> DKA Osmolal gap: - Ethylene glycol (urinary calcium oxalate crystals) - Methanol (blindness) - Propylene glycol

IgA nephropathy

Clinical presentation: - Usually within 5 days of URI - More common in young adults - Recurrent gross hematuria Dx: - Normal serum complement - Mesangial IgA deposits seen in renal Bx Prognosis: - Usually benign - RPGN or nephrotic syndrome w/ worse prognosis

Calcium phosphate stones

Common in primary hyperparathyroidism and renal tubular acidosis

Overflow incontinence

Constant involuntary dribbling of urine & incomplete emptying. Neurogenic bladder Tx: - Cholinergic agonists (bethanechol) - Intermittent catheterization for retention

Hyponatremia correction

Correction of serum sodium should not exceed 0.5 mEq/L/hr to avoid osmotic demyelination or central pontine myelinolysis. Excess water being moved by osmosis from the intracellular compartment into extracellular compartment. This could lead to disruption of cellular metabolic activity and subsequent cell damage Note: opposite can happen when correcting hypernatremia (cerebral edema could occur)

Diabetic nephropathy

DM leading cause of ESRD in US Disease progression can be slowed with strict glycemic control, tx of HTN, and angiotensin blockade. Histology: diffuse glomerulosclerosis - Nodular glomerularsclerosis (Kimmelsteil-Wilson nodules) is pathognomonic 1st year DM: - Glomerular hyperperfusion and renal hypertrophy with increase in GFR 5 years DM: - GBM thickening, glomerular hypertrophy, mesangial volume expansion - GFR returns to normal 5-10 years DM: - Microalbuminuria - Overt nephropathy

Renin angiotensin aldosterone system (RAAS)

Decreased RBF --> decreased GFR --> justaglomerular apparatus increases renin --> promotes angiotensinogen production from liver --> increased angiotensin I --> ACE (lungs) converts to angiotensin II --> stimulates: - Sodium retention (direct effect) directly increases proximal tubule sodium reabsorption - Aldosterone production increases sodium and water reabsorption in distal tubule - Vasoconstriction increases efferent and systemic arteriolar resistance to improve GFR and BP

Primary adrenal insufficiency (Addison's disease)

Decreased cortisol, adrenal sex hormone, and aldosterone secretion Etiology: - Autoimmune - Infectious (TB, HIV, disseminated fungal) - Hemorrhagic infarction (meingococcemia, anticoagulants) - Metastatic ca p/w: - Shock, fever, n/v, weight loss, anorexia - Abdominal tenderness w/ deep palpation - Hyponatremia, hyperkalemia, hypercalcemia, hypoglycemia, eosinophilia - Fatigue, weakness - Hyperpigmentation or vitiligo - Hypotension - Anemia - Normal AG acidosis Dx: - Measure ACTH and serum cortisol with high-dose ACTH stimulation test - Primary adrenal insufficiency will have low cortisol, high ACTH - Secondary/tertiary adrenal insufficiency will have low cortisol and low ACTH

Prerenal azotemia--AKI

Decreased renal perfusion: - True volume depletion - Decreased EABV (HF, cirrhosis) - Displacement of intravascular fluid (sepsis, pancreatitis) - Renal artery stenosis - Afferent arteriole vasoconstriction (NSAIDs) Clinical features: - Elevated creatinine - Elevated BUN w/ BUN:Cr > 20:1 - Decreased urine output - FeNa < 1% - Unremarkable urine sediment AG metabolic acidosis possible 2/2 uremia

Familial hypocalciuric hypercalcemia (FHH)

Decreased sensitivity to Ca. Due to mutation in calcium sensing receptor (CaSR). Higher calcium levels required to suppress PTH release. Defective CaSR leads to increased reabsorption of Ca in renal tubules. - High/normal PTH - Low urinary Ca excretion Urine calcium/Cre clearance ratio (UCCR): (Urine Ca/Serum Ca)/(Urine Cr/Serum Cr) Complications: - Pancreatitis - Chondrocalcinosis Note: cinacalcet increases sensitivity to Ca

Bartter syndrome

Defect in salt reabsorption in thick ascending loop of Henle - Chronic volume depletion - Hyperplasia of JGA - Increased renin levels and secondary aldosterone elevations

Crystal-induced AKI

Drug has low urine solubility. Precipitates in tubules, causing intratubular obstruction and direct renal tubular toxicity. Cause: - Acyclovir - Sulfonamides - Methotrexate - Ethylene glycol - Protease inhibitors - Uric acid (tumor lysis syndrome) p/w: - Asymptomatic - AKI < 7d of starting drug - UA: hematuria, pyuria, crystals - Increased risk with volume depletion, CKD Management: - d/c drug - Volume repletion - Loop diuretic

Humoral hypercalcemia of malignancy

Due to secretion of PTHrp from malignant cells. Severe: weakness, GI distress, neuropsychiatric symptoms. Usually volume depleted 2/2 polyuria from hypercalcemia-induced nephrogenic diabetes insipidus and decreased oral intake

Uncomplicated cystitis

Dysuria, urinary frequency, suprapubic tenderness. - Nitrofurantoin for 5d (aboid in suspected pyelonephritis or creatinine clearance < 60 mL/min) - TMP-SMX for 3d (avoid if local resistance rate > 20%) - Fosfomycin single dose - Fluoroquinolones (only if above options can't be used) - UCx only needed if initial treatment fails

Uric acid stones

Formed when urine is acidic or when there is increased cell turnover (results in hyperuricemia and hyperuricosuria). Needle-shaped crystals on UA. Radiolucent Dehydration also increases risk Evaluation: CT abdomen, US, or IV pyelography

Struvite stones

Formed with urine is alkaline because of infection with urease producing bacteria (proteus)

Interstitial cystitis (painful bladder syndrome)

Epidemiology: - More common in women - Associated with psychiatric disorders (anxiety) and pain syndromes (fibromyalgia) p/w: - Bladder pain with filling--relief with voiding - Increased frequency and urgency - Dyspareunia - Pain can be exacerbated by exercise and EtOH Dx: - Bladder pain with no attributable cause for > 6 weeks - Normal UA Tx: - Focus on quality of life - Behavioral modification & trigger avoidance - Amitriptyline - Analgesics for exacerbations

SIADH

Etiologies: - CNS disturbance - Medications (carbamazepine, SSRIs, NSAIDs) - Lung disease - Ectopic ADH secretion (small cell lung ca) - Pain &/or nausea Clinical features: - Mild/moderate hyponatremia (nausea, forgetfulness) - Severe hyponatremia (seizures, coma) - Euvolemia (moist mucous membranes, no edema, no JVD) Lab findings: - Hyponatremia - Low serum osmolality < 275 (hypotonic) - High urine osmolality > 100 - High urine sodium > 40 - Serum uric acid is low Management: - Fluid restriction +/- salt tablets - Hypoertonic (3%) saline for severe hyponatremia - Infusion of saline must have a higher electrolyte concentration than that of urine

Diabetes insipidus

Euvolemic hypernatremia - Euvolemia - Polyuria - Mild hypernatremia Complete DI: urine osmolality less than 300 mOsm/kg (often less than 100) Partial DI: urine osmolality from 300-600 Serum osmolality elevated in both types Central DI: due to decreased production of ADH. Common causes include trauma, hemorrhage, infection, tumors Nephrogenic DI: results from renal ADH resistance. Common causes include hypercalcemia, severe hypokalemia, tubulointerstitial renal disease, medications (lithium, demeclocycline, foscarnet, cidofovir, amphotericin)

Psychogenic polydipsia

Excessive free water intake 2/2 psychiatric condition - Euvolemia - Polyuria (dilute urine) - Hyponatremia (as opposed to hyperNa with DI)

Analgesic nephropathy

Generally seen after cumulative ingestion of 2-3 kg of the index drug. Papillary necrosis and chronic tubulointerstitial nephritis are the most common pathologies. - Polyuria, sterile pyuria - Microscopic hematuria - Renal colic following sloughing of renal papilla - HTN - Mild proteinuria - Impaired urinary concentration - Elevated creatinine - CT shows small kidneys with b/l renal papillary calcifications Chronic analgesic abuse can lead to premature aging, atherosclerotic vascular disease, urinary tract cancer.

Nonglomerular hematuria

Gross > microscopic Nepholithiasis Cancer (renal, prostate) Polycystic kidney disease Infection (cystitis) Papillary necrosis p/w: dysuria, urinary obstruction UA: blood but no protein - Normal RBCs

Renal tubular acidosis

Group of disorders characterized by non-AG metabolic acidosis in the presence of preserved kidney function Proximal RTA (type 2): defective tubular bicarb reabsorption in the proximal tubules - Often associated with Fanconi syndrome - Can also occur due to carbonic anhydrase inhibitors Hyperkalemic RTA (type 4): cortical collecting tubule is the site for H and K excretion (regulated by aldosterone). Impaired function of the cortical collecting tubule due to aldosterone def. or resistance will cause retention of H and K. - RTA type 4 commonly seen in elderly pts who have poorly controlled DM with damage to the juxtaglomerular apparatus - Causes state of hyporeninemic hypoaldosteronism - Mild hyperkalemia, mild acidosis, background of mildly diminished GFR

Cardiovascular risk factors

HTN, DM, low HDL, LVH, CAD, age Related to ESRD: - ESRD - Anemia - Metabolic abnormality (hyperphosphatemia, and increased PTH levels) - Increased homocysteine levels (impaired metabolism and decreased removal) - Accelerated atherogenesis in dialysis pts (ebhanced oxidant stress due to uremia and bio-incompatible renal replacement therapies) - Increased calcium intake (given to correct hyperphosphatemia) that enhances coronary artery calcification - Inhibition of NO )cause vasoconstriction and HTN

Primary hyperaldosteronism

High aldosterone causes increased H and K excretion, leading to hypokalmeia and metabolic alkalosis ASSPP: Aldosterone Saves Sodium Pushes Potassium out

Nephrosclerosis

Hypertrophy and intimal medial fibrosis of renal arterioles

Chronic alcoholism (electrolyte imbalances)

Hypomagnesemia - Poor PO intake - Alcohol induced renal losses - Diarrhea Hypophosphatemia - Weakness - Rhabdomyolysis - Paresthesias - Respiratory failure Hypomagnesemia can cause refractory hypokalemia: - Intracellular Mg inhibits potassium secretion by ROMK channels in the collecting tubules of the kidney - Therefore, low Mg leads to excessive tubular secretion of K - Tx with both Mg and K repletion

Pancreatitis

Hypovolemia due to: - Vomiting - Inability to tolerate oral fluids - Third space extravasation p/w: dry mucus membranes, hemoconcentration, tachycardia, hypotension, shock

Adrenal insufficiency

Hypovolemia, which leads to increased ADH and hyponatremia Loss of aldosterone: - Increased sodium excretion - Increased potassium/hydrogen retention

Cerebral salt wasting

Hypovolemic hyponatremia - High urine sodium (> 20 mEq/L) Occurs 2/2 neurological insult (injury/surgery)

Management of oliguria (< 250 mL in 12 hr)

If urinary retention: - Uretheral cath - Serum and urine biochemistry + imaging - Treat underlying cause (BPH, malignancy) If no urinary retention: - Serum & urine biochemistry + imaging - Prerenal causes: - Hypovolemia - Sepsis - Low CO (HF w/ volume overload-- cardiorenal syndrome ) - Fluid administration or tx underlying cause - Renal causes: - ATN - Interstitial nephritis - Glomerular disease - Treat underlying cause

Causes of peripheral edema

Increased capillary hydrostatic pressure: - Heart failure (LV & cor pulmonale) - Primary renal sodium retention (renal disease & drugs) - Venous obstruction (cirrhosis, venous insufficiency) Decreased oncotic pressure (hypoalbuminemia): - Protein loss (nephrotic syndrome & protein-losing enteropathy - Decreased albumin synthesis (cirrhosis, malnutrition) Increased capillary permeability: - Burns, trauma, and sepsis - Allergic reactions - ARDS - Malignant ascites Lymphatic obstruction/increased interstitial oncotic pressure: - Malignant ascites - Hypothyroidism - Lymph node dissection

Cystinuria

Inherited group of disorders characterized by impaired transport of dibasic AAs (cystine, lysine, arginine, ornithine) by the brush borders of renal tubular and intestinal epithelial cells. Cystine is poorly soluble in water, leading to formation of hard (radiooppaque) renal stones - h/o recurrent stones since childhoos - Family history - Hexagonal crystals on UA - Positive urinary cyanide nitroprusside test (detects elevated cystine levels)

Hyperkalemia

K > 5 mEq/L Causes: - AKI, CKD - Medications (see above) - Disorders that impair the RAAS - Increased potassium movement out of cells (uncontrolled hyperglycemia, metabolic acidosis) - Increased tissue metabolism (trauma, tumor lysis syndrome) Symptoms: - Ascending muscle weakness w/ flaccid paralysis - ECG changes (peaked T waves, followed by short QT intervals, QRS widening, prolonged PR, sine wave with v-fib, conduction blocks, ectopy, sine wave pattern) - Bradycardia Tx: - Calcium gluconate (cardiac stabilization) - Insulin with glucose, sodium bicarb, Beta-2 adrenergic agonists (rapid) - Dialysis, kayexalate, diuretics (excretion) Note: uncontrolled chronic hyperkalemia may be asymptomatic until the potassium rises above 7 Note: Inhaled beta agonists can cause tachycardia and precipitate angina in pts with CAD

Stress incontinence

Leaking with coughing, sneezing, laughing, and lifting Tx: - Lifestyle modification - Pelvic floor exercises - Pessary - Pelvic floor surgery - Duloextine (SNRI)

Glomerular hematuria

Microscopic > gross Glomerulonephritis - Post-strep - IgA nephropathy BM disorder - Alport syndrome Usually nonspecific or no sxs. Can present with nephritic syndrome (hematuria, HTN, oliguria, elevated creatinine). UA: blood & protein - RBC casts, dysmorphic RBCs

Autosomal dominant polycystic kidney disease

Most common cause of inherited renal disease in adults. ESRD by age 60 p/w abdominal/flank pain with microscopic or gross hematuria. HTN. UTIs, nephrolithiasis

Glomerulosclerosis

Progressive loss of glomerular capillary surface area with glomerular and peritubular fibrosis

Medications that cause hyperkalemia

Nonselective beta-blockers - Interferes with beta-2-mediated intracellular potassium uptake ACE inhibitor, ARB, K sparing diuretics - Inhibition of aldosterone or the ENaC channel Digitalis - Inhibition of the Na-K-ATPase pump Cyclosporine - Blocks aldosterone activity Heparin - Blocks aldosterone production NSAIDs - Decreases renal perfusion resulting in decreased K deliver to the collecting ducts Succinylcholine - Causes extracellular leakage of potassium through acetylcholine receptors Trimethoprim - Blockade of the epithelial sodium channel in the collecting tubule - Also competitively inhibits renal tubular creatinine secretion and may cause artificial increased in serum creatinine without changing GFR

Osmolal gap

OG = measured serum osmolality - calculated serum osmolality Calculated serum osmolality = 2(Na) + glucose/18 + BUN/2.8

Post-infectious glomerulonephritis

Occurs 1-2 wks after an episode of strep pharyngitis/skin infection (not after UTI) More common in children, but can occur in adults - Gross hematuria - Oliguria - Mild proteinuria - RBC casts - Fluid retention and HTN - Periorbital edema - Serum C3 complement levels are low - Elevated anti-streptolysin O and/or anti-DNAse B - Subepithelial humps on renal Bx Prognosis: - Children have good prognosis - Possible chronic kidney disease in adults

Hemolytic uremic syndrome

Occurs after infection with Shiga-toxin-producing E coli. - Microangiopathic hemolytic anemia - Thrombocytopenia - Renal failure from thrombotic aniopathy

Winter's formula

PaCO2 = 1.5(HCO3) + 8(+/-2) Expected change in PaCO2 during metabolic acidosis 2/2 hyperventilation (Kussmaul breathing) via chemoreceptor response to blow off CO2.

Fractional excretion of sodium (FENa)

Percentage of the sodium filtered by the kidney which is excreted into the urine. FENa = 100((urine Na * plasma Cr)/(plasma Na * urine Cr)) FENa = Na clearance / GFR Low FENa indicates sodium retension by the kidney, suggesting prerenal disease. High FENa suggests sodium wasting due to ATN or other intrinsic kidney diseases Note: FENa invalidated by diureetic use

Henoch-Schonlein purpura

Presentings in childhood as palpable purpura on the buttocks w/ abdominal pain, arthralgias, proteinuria, and hematuria w/ RBC casts on UA Serum complement normal and not associated with HCV

Acid-base disorders

Primary metabolic acidosis compensation: - PaCO2 = 1.5(HCO3)+8 +/- 2 Primary metabolic alkalosis compensation: - Increased PaCO2 by 0.7 mmHg for every 1 mEq/L rise in serum HCO3 Primary respiratory acidosis compensation: - Increase serum HCO3 by 1 mEq/l for every 10 mmHg rise in PaCO2 Primary respiratory alkalosis compensation: - Decrease in serum HCO3 by 2 mEq/L for every 10 mmHg decrease in PaCO2

Unilateral obstructive uropathy

Renal calculi - Flank pain (renal capsular distension) - Poor urine output (mechanic outflow obstruction) Intermittent episodes of high-volume urination can occur when obstruction is overcome by large volume of retained urine (post-obstructive diuresis). Excessive diuresis may lead to potassium wasting and dehydration. Both can cause weakness. b/l functional kidneys more likely to have post-obstructive diuresis as the affected kidney will produce large volume of urine once obstruction cleared. Single kidneys are more likely to develop AKI w/ obstruction Tx: stones < 1 cm may pass spontaneously with hydration and alagesia; otherwise surgery

Multiple myeloma

Renal insufficiency 2/2 obstruction of the distal collecting tubules by large casts of Bence-Jones proteins Amyloid deposition and infiltration of kidney by plasma cells also common

Evaluation of hyponatremia

Serum osmolality > 290: - Marked hyperglycemia - Advanced renal failure Serum osmolality < 290 with urine osmolality < 100: - Primary polydipsia - Malnutrition (beer drinker's potomania) Serum osmolality < 290 with urine osmolality > 100 and urine sodium < 25: - Volume depletion - CHF - Cirrhosis Serum osmolality < 290 with urine osmolality > 100 and urine sodium > 25: - SIADH - Adrenal insufficiency - Hypothyroidism

Iatrogenic hyponatremia

Risks: - Hypotonic fluid hydration - Children, premenopausal women, eldrly - Hypoxia - CNS d/o p/w; - HA - n/v - Encephalopathy ( AMS, seizure) Management: - Hypertonic (3% saline) - Serial measurement of electrolytes - Increase serum sodium 6-8 mEq/L in first 24 hrs

Metabolic alkalosis

Saline responsive: - Vomiting - Gastric suctioning - Diuretics - Laxative abuse - Decreased PO fluid intake (volume depletion) Saline resistant: - Primary hyperaldosteronism - Cushing's syndrome - Severe hypokalemia (<2 mEq/L) p/w: - Volume depletion (fatigue, postural dizziness, muscle cramps) - Hypokalemia (muscle weakness, arrhythmias) - Urine chloride (< 20 is saline responsive; > 20 is saline resistant) Tx: - Treat underlying cause to reverse generation phase in all cases - Saline responsive (also give normal saline to correct maintenance phase) Generation phase (saline-responsive): Urinary/GI hydrogen loss (diuretics/vomiting) or decrease PO intake. Generation of excess bicarbonate. Maintenance phase (saline-responsive): hypovolemia prevents the normal kidney from excreting the excess bicarbonate in urine. Prerenal also causes aldosterone excretion. Potassium wasting and hydrogen wasting.

Post-ictal lactic acidosis

Seizure activity, especially tonic-clonic seizures, can significantly raise serum lactic acid due to skeletal muscle hypoxia and impaired hepatic lactic acid uptake Results in transient AG metabolic acidosis - Usually resolves w/in 90 min

Hepatorenal syndrome

Sever liver damage --> increased NO generation in splanchnic circulation 2/2 portal HTN --> systemic vasodilation --> reduces BP --> renal hypoperfusion --> activation of compensatory pathways (RAAS, sympathetic nervous system, ADH) --> increase water/Na retention --> worsen volume overload Risk factors: advanced cirrhosis w/ portal HTN Precipitating factors: - Reduced renal perfusion - GI bleed, vomiting, sepsis, excessive diuresis, spontaneous bacterial peritonitis - Reduced GFR (NSAIDs) Dx: - Renal hypoperfusion (prerenl labs) - FeNa < 1% (or urine Na < 10 mEq/L) - Absence of tubular injury - No RBC, protein, or granular casts in urine - No improvement of renal function with fluids Tx: - Address precipitating factors (hypovolemia, anemia, infection) - Splanchnic vasoconstrictors (midodrine, octreotide, NE) - Liver transplantation

Management of hypercalcemia

Severe (Ca > 14 mg/dL) or symptomatic: - Normal saline hydration plus calcitonin - Avoid loop diuretics unless volume overload (CHF) exists - Bosphosphonate (zoledronic acid) --> Long-term Moderate (Ca 12-14): - Usually no immediate tx required unless symptomatic - Tx similar to severe hypercalcemia Asymptomatic or mild (Ca < 12): - No immediate tx - Avoid thiazide diuretics, lithium, volume depletion, and prolonged bed rest HD if renal failure or severe CHF that can't get IVF Note: glucocorticoids can be used to treat hypercalcemia due to excessive vitamin D intake, granulomatous diseases, and certain lymphomas because it inhibits formation of activated vitamin D by mononuclear cells

Renal papillary necrosis

Sloughing of the renal papilla. Rare NSAID: - NSAIDs - SCD - Analgesic abuse (tylenol) - Infection - DM

Urge incontinence

Sudden, overwhelming/frequent need to empty the bladder. Detrusor overactivity Risk factors: - 40+ - Female - Pelvic surgery Tx: - Lifestyle modification - Bladder training - Antimuscarinic drugs (oxybutynin)

Pyelonephritis

UTI with fever, flank pain/tenderness, rigors - Pyuria - Bacteriuria Outpt: fluoroquinolones (cipro, levo) Inpt: IV abx (fluoroquinolone, aminoglycoside +/- ampicilliN) - Obtain sample for urine culture prior to initiating therapy and adjust abx as needed

Aspirin intoxication

Tinnitus, fever, tachypnea, nausea, GI irritation Respiratory alkalosis: stimulation of respiratory center in medulla causing tachypnea AG metabolic acidosis: uncoupling of oxidative phosphorylation in the mitochondria leading to anaerobic metabolism (results in low bicarb from acid buildup). Also decreased renal excretion of organic acids ABG: - Low PaCO2 due to primary respiratory alkalosis and respiratory compensation for metabolic acidosis) - Low HCO3 due to primary metabolic acidosis and for metabolic compensation of respiratory alkalosis) - Arterial pH may be normal as the two acid-base disturbances shift pH in opposite directions Over time, metabolic acidosis worsens and the pt will reach a point at which they cannot ventilate quickly enough to compensate. Tx: alkalinization or dialysis

Septic hypotension

Treat with IVF (isotonic saline). Will improve prerenal azotemia. Clinical condition may worsen before improving if pt develops ATN or septic shock. Avoid nephrotoxins: - NSAIDs - Metformin (can cause lactic acidosis in AKI, liver failure, and sepsis) - ACEIs/ARBs (temporarily worsen renal function and hypotension in AKI)

Hydronephrosis/hydroureter

Typical sign of urinary obstruction

Renal artery stenosis

Typically due to atherosclerotic disease p/w difficult to control HTN w/wo renal dysfunction. - Resistant HTN (3-drug) - Malignant HTN (with end organ damage) - Onset of severe HTN (>180/120) after age 55 - Severe HTN w/ diffuse atherosclerosis - Recurrent flash pulmonary edema w/ severe HTN PE/Labs/imaging: - Asymmetric renal size - Abdominal bruit - Unexplained rise in Cr after starting ACEI or ARBs - Unexplained atrophic kidney Tx: risk factor reduction - Aspirin, DM & HLD control, smoking cessation - ACEI/ARB

Hypovoemic hypernatremia

Water deficit in relation to sodium. Occurs with hypotonic fluid loss and decreased access to free water. Tx: isotonic 0.9% saline (initially hypoosmolar to the hypernatremic plasma) - Once the volume deficit has been restored, pts are then switched to half-normal 0.45% saline in order to better replace the free water deficit - Goal rate of plasma sodium correction is no more than 1 mEq/L/hr (to avoid cerebral edema)

Alport syndrome

X-linked defect in collagen IV formation p/w: - Hearing loss - Ocular abnormalities - Hematuria - Progressive renal insufficiency Renal Bx shows thinning of glomerular BM

Metabolic alkalosis DDx

pH > 7.45 & HCO3 > 24 mEq/L If low urine chloride: - Vomiting/nasogastric aspiration (saline) - Prior diuretic use (saline) If high urine chloride: (hypo/euvolemia) - Current diuretic use (saline) - Loops and thiazides cause chloride loss and volume contraction - Bartter & Gitelman syndromes If high urine chloride: (hypervolemia) - Excess mineralocorticoid activity - Primary hyperaldosteronism - Cushing disease - Ectopic ACTH production