Uro/Renal Flashcards
Metabolic Acidosis mudpiles
High-Anion Gap ⇢ MUDPILES
#MCC + ingestions
M: methanol (formic acid)
U: uremia (AKI/CKD, rhabdomyolysis)#
K: ketoacidosis (diabetic, alcoholic, starvation)#
P: propylene glycol
I: iron/isoniazid
L: lactic acidosis
E: ethylene glycol (oxalic acid)
S: salicylates (e.g., ASA)
Lactic Acidosis:
*Type A: related to hypoxia (e.g., septic or hypovolemic shock, hypoxemia, carbon monoxide poisoning)
*Type B: not related to hypoxia (e.g., liver failure, seizures, ETOH/methanol intoxication, isoniazid)
Metabolic Acidosis primary disturbance vs compensation
Primary Disturbance: ⇣ pH (<7.4), ⇣ HCO3 (<24)
*loss of bicarb or gain of H+
Calculate anion gap: [Na] – [Cl + HCO3]
*high-anion gap (>12mEq/L) ⇢ “MUDPILES” ⇢
*normal (6-12mEq/L) ⇢ calculate UAG
UAG: [urine Na] + [urine K] – [urine Cl]
*⊖UAG ⇢ GI HCO3 loss (diarrhea) ⇢
*⊕UAG ⇢ RTA (⇣ renal acid excretion)
Respiratory Compensation: ⇡ RR ⇢ hyperventilation = ⇣ PCO2 (<40)
Expected PCO2: ⇣ [PCO2] 1.3mmHg per 1mEq/L ⇣ [HCO3]
*full compensation expected within 12-24h
DX: ketones, lactate, BUN/creatinine +/- tox screen
TX: directed at underlying cause (lactic acidosis, ketoacidosis, etc.)
*renal failure: give alkali (NaHCO3, sodium citrate) +/- dialysis
*ethylene glycol/methanol OD: fomepizole + HD
TX: Na, K, & HCO3 repletion PRN
TX: correct metabolic abnormalities to prevent nephrocalcinosis/CKD
*Distal: NaHCO3, often requires K supplementation
*Proximal: NaHCO3 or KHCO3 (more needed), thiazide diuretic
*⇡⇡ K: fludrocortisone, restrict dietary K, furosemide, NaHCO3
Metabolic Alkalosis causes
*volume depletion & hypokalemia are MC stimuli for ⇡ HCO3 reabsorption
Chloride Responsive (urine Cl <20mEq/L): chloride/ECFV loss, Cl repletion = correction
*Contraction alkalosis: ▪loop/thiazide diuretics, sweat loss in cystic fibrosis
▪︎vomiting/NG suction (HCl loss), congenital chloride diarrhea
*Renal H+ loss:
▪︎post-hypercapnia
Chloride Unresponsive (urine Cl >20mEq/L): severe K/Mg ⇣ or mineralocorticoid ⇡⇡, Cl repletion ≠ correction
*Mineralocorticoid excess:
▪︎1°/2° aldosteronism, congenital adrenal hyperplasia, hyperreninism
⊕HTN
▪︎CHF, cirrhosis w/ ascites, nephrotic syndrome
▪︎Liddle’s: pseudohypoaldosteronism (epithelial Na channel defect)
▪︎glycyrrhizic acid (licorice) ingestion (mimics mineralocorticoid excess)
*Genetic ion transport d/o:
▪︎Bartter ⇢ NaCl reabsorption defect in loop of Henle (mimics loops)
⊘HTN (normo/hypo)
▪︎Gitelman ⇢ NaCl reabsorption defect in DCT (mimics thiazides)
Metabolic Alkalosis primary disturbance and compensation
Primary Disturbance: ⇡ pH (>7.4), ⇡ HCO3 (>24)
*loss of H+ or gain of bicarb
Urinary Cl <20mEq/L ⇢ chloride responsive ⇢
Urinary Cl >20mEq/L ⇢ chloride unresponsive ⇢
*Urinary K <30mEq/L ⇢ laxative abuse, severe ⇣ K
*Urinary K >30mEq/L ⇢ look at BP
⊘HTN: Bartter, Gitelman
⊕HTN: consider mineralocorticoid excess
Respiratory Compensation: ⇣ RR ⇢ hypoventilation = ⇡ PCO2 (>40)
Expected PCO2: ⇡ [PCO2] 0.7mmHg per 1mEq/L ⇡ [HCO3]
*full compensation expected within 12-24h
TX: IV 0.9% NaCl (NS), treat underlying cause
TX: patients w/ severe alkalosis (pH >7.6) sometimes require more urgent correct of blood pH
*hemodialysis an option if volume overloaded + renal dysfunction
*Acetazolamide 250-375mg ⇡ HCO3 excretion but may also
accelerate urinary losses of potassium & phosphate
Respiratory Acidosis (hypercapnia) acute vs chronic
ACUTE:
*acute lung disease (e.g., pneumonia, pulmonary edema), acute COPD/asthma exacerbation
*CNS depression d/t head trauma, postictal state, drugs (e.g., opiates, BDZs), OSA
S/SXS: HA, confusion, anxiety, drowsiness, tremor, blunted DTRs, myoclonic jerks, asterixis +/- papilledema
CHRONIC:
*airway obstruction (e.g., COPD/asthma)
*respiratory muscle weakness (e.g., Myasthenia gravis, ALS, Guillain-Barre, Multiple Sclerosis)
S/SXS: may be well tolerated, but may have memory loss, sleep disturbances, excessive daytime sleepiness, personality changes
Respiratory Acidosis primary vs compensation
Primary Disturbance: ⇣ pH (<7.4), ⇡ PCO2 (>40)
*hypoventilation (retain CO2)
ACUTE TX:
*noninvasive ventilation (BiPAP) to blow off CO2
*invasive ventilation (trach) sometimes needed
*Naloxone for opioid OD
Metabolic Compensation: ⇡ HCO3 reabsorption (>24)
Expected HCO3, Acute: ⇡ [HCO3] 1mEq/L per 10mmHg ⇡ [PCO2]
Expected HCO3, Chronic: ⇡ [HCO3] 3.5mEq/L per 10mmHg ⇡ [PCO2]
*full compensation expected within 3-5d
CHRONIC TX:
*directed at underlying cause
*chronic hypercapnia must be corrected slowly (i.e., over hours to
minutes) because lowering PCO2 too rapidly can cause post-
hypercapnic “overshoot” alkalosis ⇢ seizures, death
Respiratory Alkalosis acute vs chronic
ACUTE: **think ⇢ pain, anxiety, or hypoxemia (e.g., high altitude, pneumonia, PE, ARDS)
*fever, sepsis, stroke, seizures (postictal)
*mechanical overventilation, drugs (e.g., salicylates, theophylline, progesterone)
S/SXS: lightheadedness, confusion, peripheral/circumoral paresthesias, cramps, syncope
*hypocalcemia ⇢ carpopedal spasms
CHRONIC: PE during pregnancy, liver failure, hyperthyroidism, brainstem tumor
S/SXS: asymptomatic, no specific signs
Respiratory Alkalosis primary vs compensation
Primary Disturbance: ⇡ pH (>7.4), ⇣ PCO2 (<40)
*hyperventilation (blow off CO2)
Metabolic Compensation: ⇣ HCO3 reabsorption (<24)
Expected HCO3, Acute: ⇣ [HCO3] 2mEq/L per 10mmHg ⇣ [PCO2]
Chronic: ⇣ [HCO3] 5mEq/L per 10mmHg ⇣ [PCO2]
TX: directed at underlying cause
*not life-threatening, pH lowering interventions not needed
*DISCOURAGE paper bag breathing ⇢ doesn’t fix PCO2 & may ⇣ PO2
AKI definition, sx, dx, tx
AKI: sudden loss of renal function w/ subsequent BUN/Cr ⇡
Defined as any of the following: ➀ SCr ⇡ ≥0.3mg/dL within 48h ➁ SCr ⇡ ≥1.5x baseline within 7d ➂ Urine output <0.5mL/kg/h for ≥6h
S/SXS: symptoms of uremia may develop later as nitrogenous
products accumulate ⇢ anorexia, N/V, weakness, confusion,
myoclonic jerks, seizures, coma
PE: +/- asterixis & hyperreflexia
» Uremic pericarditis: pleuritic CP worse when supine, improves w/ leaning forward
▪︎⊕pericardial friction rub
Phase:
➀ Onset phase
▪︎S/SXS of underlying cause may be present, urine output <0.5mL/kg/h Hours-days
(kidney injury)
➁ Oliguric/Anuric phase
▪︎progressive deterioration of kidney function
1-3wks (maintenance phase)
» oliguria (urine output <400mL/d); <50mL/d = anuria
» ⇡ BUN & creatinine (azotemia)
▪S/SXS: volume overload (e.g., peripheral & pulmonary edema, HF, HTN), metabolic acidosis, hyperkalemia, uremic symptoms
➂ Diuretic phase
▪︎GFR returns to normal, urine production ⇡ (polyuria), but tubular ~2wks reabsorption remains disturbed (i.e., can excrete but not concentrate urine) ⇢ fluid/electrolyte loss: hyponatremia, hypokalemia, dehydration)
➃ Recovery phase ▪︎normalization of kidney function & urine production Months-1y
Prerenal AKI causes, dx, tx
*MCC of AKI
PATHO: any condition that leads to decreased renal perfusion (MCC, ~60%)
» Hypovolemia: GI loss (e.g., V/D, bleeding), renal losses (e.g., diuretics), sweat/burns, 3rd-spacing
» Hypotension: shock (e.g., hypovolemic, myocardial, septic)
» Edematous states: heart failure (⇣ CO), cirrhosis
» Afferent (preglomerular) arteriolar dilation (e.g., NSAIDs, calcineurin inhibitors)
» Efferent (postglomerular) arteriolar constriction (e.g., ACEI/ARBs)
dx
▪︎BUN/Cr ratio >20:1
▪︎FENA <1%
▪︎UNa <20mEq/L
▪︎urine osmolality >500mOsm/kg
▪︎urinary sediment ⇢ hyaline casts
tx
▪︎IV fluid resuscitation for hypovolemia
▪︎DC offending drugs
▪︎hemodynamic support as indicated (e.g., shock)
*rapid improvement in w/ acute intervention
Postrenal AKI definition, dx, tx
PATHO: bilateral obstruction of urinary flow from renal pelvis to urethra
» Acquired obstructions (e.g., BPH, catheter injuries, tumors, stones, bleeding w/ clot formation)
» Neurogenic bladder (e.g., multiple sclerosis, spinal cord lesions, peripheral neuropathy)
» Congenital malformations (e.g., posterior urethral valves)
dx
▪︎⇡ creatinine in bilateral obstruction
▪︎urine osmolality <350mOsm/kg
▪︎postvoid residual volume >200mL suggests BOO
▪︎urinary sediment ⇢ normal, red cells, white cells, or crystals
*BUN/Cr ratio, FENA, & UNa vary
Renal U/S ⇢ hydroureter/hydronephrosis
tx
Bladder outlet obstruction (BOO):
▪︎urethral catheterization to relieve obstruction
Ureteral or renal pelvic obstruction:
▪︎ureteral stenting, percutaneous nephrostomy
*rapid improvement w/ obstruction relief
Acute Tubular Necrosis causes, dx, tx
*MC intrinsic AKI
ATN: caused by either ischemic damage or toxins; tubules necrose, die, & slough off
» Ischemic: renal hypoperfusion most often caused by hypotension or sepsis
» Nephrotoxins: IV contrast, aminoglycosides, amphotericin B, NSAIDs, cyclosporine, vancomycin
▪︎Heme pigments: myoglobinuria (rhabdomyolysis), hemoglobinuria (hemolysis)
▪︎Endogenous toxins: uric acid (tumor lysis syndrome), Bence-Jones proteins (multiple myeloma)
dx
▪︎BUN/Cr ratio <20:1 ▪︎FENA >1%
▪︎urine osmolality <350mOsm/kg ▪︎UNa >20mEq/L
▪︎urinary sediment ⇢ muddy brown granular casts, renal tubular epithelial cells
tx
▪︎DC any potential nephrotoxins
▪︎supportive therapy w/ IV fluids
» Oliguric: strict fluid balance monitoring
» Polyuric: replace fluid/electrolyte losses
Acute Interstitial Nephritis definition, sx, dx, tx
AIN: inflammatory infiltrate & edema affecting the renal interstitium; develops over days to months
▪︎inflammatory infiltrates ⇢ tissue edema & tubular cell damage ⇢ compromised tubular flow
▪︎allergic: drugs act as haptens ⇢ type IV hypersensitivity reaction
» Medications (MCC): β-lactams (e.g., ciprofloxacin, isoniazid), macrolides (e.g., vancomycin,
rifampin), NSAIDs, anticonvulsants (e.g., CBZ, phenytoin, valproate)
» Bacterial infections: Brucella, Legionella, Mycobacterium, Salmonella, staph/strep
» Viral infections: CMV, EBV, HCV, HIV, mumps
» Autoimmune: Sjogren syndrome, sarcoidosis, SLE, cryoglobulinemia
dx
S/SXS: AKI +/- morbilliform rash, fever, arthralgias, flank pain
▪︎BUN/Cr ratio <20:1
▪︎urinary sediment ⇢ white cells, white cell casts +/- eosinophils
tx
▪︎DC causative agents, treat underlying disease
▪︎AKI supportive therapy x3-5d
Glucocorticoids ⇢ indications:
▪︎drug-induced AIN, autoimmune AIN
▪︎postinfectious AIN w/ delayed recovery
▪︎insufficient GFR ⇡ after 3-5d of supportive TX
▪︎impending indication for dialysis
▪︎diffuse infiltrates w/o extensive fibrosis on BX
Acute Glomerulonephritis types
» Poststreptococcal GN: usually affects children 3-12yo, self-limiting
▪︎occurs after group A strep infections ⇢ 1-2wks after pharyngitis (MC), 3-4wks after skin infection (impetigo)
▪DX: ⊕ASO, ⊕ADB, ⇣ C3
» IgA Nephropathy (Berger disease): MCC of AGN; young males within days (24-48h) after URI/GI infection
▪︎PATHO: IgA immune complex deposition
▪︎DX: ⇡ IgA, normal C3
▪︎S/SXS: gross hematuria & flank pain + acute URI
▪︎BX: mesangial IgA immune complex deposits
» Membranoproliferative GN (MPGN): associated w/ SLE, HCV, & cryoglobulinemia
▪︎glomerular injury d/t immune complex deposition &/or a complement-mediated mechanism
▪︎MC mixed nephritic-nephrotic syndrome
▪︎DX: ⇣ C3/C4
» Alport syndrome (hereditary nephritis): genetic defect in type IV collagen; most often X-linked, ♂︎ > ♀︎
▪︎S/SXS: isolated persistent hematuria, sensorineural hearing loss, anterior lenticonus
▪︎BX: variable thickening/thinning of GBM (basket-weave appearance)
» Rapidly progressive GN (RPGN): severe manifestations of glomerulonephritis
▪︎renal function declines rapidly over days to weeks; poor prognosis (ESRD within weeks to months)
▪︎BX: crescent formation made of plasma proteins & fibrin
➀ Goodpasture syndrome (anti-GBM antibody disease): antibodies against type IV collage of the GBM
▪︎peaks: 20-30yo (♂︎ > ♀︎), 60-70yo (♀︎ > ♂︎)
▪︎S/SXS: AGN + hemoptysis
▪︎DX: ⊕anti-GBM antibodies, normal C3
▪︎BX: linear IgG deposits along GBM
➁ Small vessel vasculitis: lack of immune complex deposition (pauci-immune)
Ⓐ Granulomatosis w/ polyangiitis (Wegener’s): ⊕C-ANCA
Ⓑ Microscopic polyangiitis: ⊕P-ANCA
dx
S/SXS: hematuria (i.e., cola-colored urine), HTN
▪︎AKI symptoms, edema (less than nephrotic)
LABS: proteinuria <3.5g/d, often ⇣ C3
AKI ⇢ ▪︎BUN/Cr ratio >20:1
▪︎UNa <20mEq/L
▪︎FENA <1%
▪︎urinary sediment ⇢ RBC casts*
tx
TX: supportive AKI therapy plus
▪︎sodium/water restriction
▪︎symptomatic azotemia: dialysis
Protein &/or HTN: ACEI/ARBs
Severe HTN &/or edema: diuretics
Poststreptococcal GN ⇢ ABX
▪︎PCN (throat), topical mupirocin (skin)
Alport: kidney transplant only definitive TX
Lupus Nephritis definition, sx, dx, tx
PATHO: mesangial/subendothelial immune complex deposition (e.g., anti-dsDNA/anti-Sm Ab), expansion/thickening of mesangium, capillary walls, &/or GBM
» Class I Minimal mesangial ▪︎S/SXS: hematuria, edema, foaming urine, HTN
» Class II Mesangial proliferative ▪︎DX: UA + creatinine, confirm w/ renal BX
» Class III Focal proliferative
» Class IV Diffuse proliferative ▪︎TX: cyclophosphamide + prednisone
» Class V Membranous
» Class VI Sclerosing
Nephrotic Syndrome definition, sx, dx, tx
Kidney disease characterized by proteinuria, hypoalbuminemia, hyperlipidemia, & edema
Membranous Nephropathy: MCC in Caucasian males >40yrs
*may be seen w/ SLE, viral hepatitis, malaria, meds (Penicillamine), hypocomplementemia
Focal Segmental Glomerulosclerosis
*in the setting of HTN, heroin, HIV
*African Americans
sx
*generalized edema (esp. periorbital in children) usually worse in the morning
*may develop frothy urine – ascites & anasarca if severe
*anemia
*DVT – loss of protein C, S, & antithrombin III + liver production of more clotting proteins
dx
UA: initial test – proteinuria causing “foamy urine,” lipiduria
*Microscopy: oval Maltese cross-shaped fat bodies (fatty casts)
*urine albumin: creatinine ratio
*24hr urine protein >3.5g/d gold standard
*hypoalbuminemia, hyperlipidemia
Renal Bx – definitive dx
*Minimal Change Disease: podocyte damage seen on electron microscope
*Membranous Nephropathy: thick basement membrane
tx
*glucocorticoids – first line for Minimal Change Disease; FSGS
Edema reduction:
*diuretics, 1L fluid & sodium restriction
Proteinuria reduction: ACEI/ARBs
Hyperlipidemia: diet modification, statins
Benign Prostatic Hyperplasia (BPH) definition, sx, dx, tx
Prostate hyperplasia (periurethral or transitional zone) leading to bladder outlet obstruction
Common in older men – hyperplasia is part of the normal aging process & is dependent on increased DHT production
sx
Irritative sxs: increased frequency, urgency, nocturia
Obstructive sxs: hesitancy, weak or intermittent stream force, incomplete emptying, & terminal dribbling
Sympathomimetics & anticholinergics may worsen the sxs
dx
DRE: uniformly enlarged, firm, nontender, rubbery prostate
PSA: normal <4ng/mL
UA: to look for hematuria or other cause of sxs
Urine cytology if increased risk of bladder cancer
tx
Mild sxs: observation (monitored annually)
Alpha blockers: best initial therapy to rapidly relieve sxs but do not change prostate size
*tamsulosin
*terazosin
*doxazosin
5-alpha reductase inhibitors: reduce the size of the prostate over 6-12mo
*finasteride, dutasteride
Surgical: TURP, laser prostatectomy
Alpha-1 Blockers MOA
Tamsulosin
Alfuzosin
Doxazosin
Terazosin
Indications: provides rapid symptom relief but no effect on the clinical course of BPH
MOA: smooth muscle relaxation of prostate & bladder neck, leading to decreased urethral resistance, obstruction relief, & increased urinary outflow
5-alpha Reductase Inhibitors MOA
Finasteride
Dutasteride
Indications: BPH & male pattern baldness
MOA: androgen inhibitor – inhibits the conversion of testosterone to DHT suppressing prostate growth, reduces bladder outlet obstruction
*doesn’t provide immediate relief but has a positive effect on clinical course of BPH (size reduction & decreases need for surgery); reduction of size in 6-12mo
Chronic Kidney Disease & ESKD definition
Normal GFR in young adults ~125mL/min/1.73m2
Etiologies: diabetes MCC of ESKD, HTN 2nd MCC
RF: DM, HTN, family hx, ≥60yo, AA, Hispanic, Asian/Pacific Islander, American Indian, NSAIDs, AKI hx
Cardiovascular disease is the leading cause of morbidity/mortality in CKD
*Kidney Failure: end stage of CKD, defined as severely ↓ kidney function OR dialysis treatment
*ESKD/ESRD (GFR <15): chronic kidney failure treated w/ either dialysis or transplantation
CKD Definition: presence of either kidney damage or ↓ kidney function for ≥3mo
Types of Structural/Functional Abnormalities:
Pathologic Abnormalities:
*Glomerular diseases (diabetes, autoimmune disease, systemic infections, drugs, neoplasia)
*Vascular diseases (atherosclerosis, HTN, ischemia, vasculitis, thrombotic microangiopathy)
*Tubulointerstitial diseases (UTI, stones, obstruction)
*Cystic disease (polycystic kidney disease, “PKD”)
Urinary sediment abnormalities:
*RBC casts, proliferative glomerulonephritis
*WBC casts, pyelonephritis or interstitial nephritis
*Oval fat bodies or fatty casts, diseases w/ proteinuria
*Granular casts & renal tubular epithelial cells in many parenchymal diseases (non-specific)
Chronic Kidney Disease & ESKD sx
CKD stages 1-4 are asymptomatic
*when GFR falls to ~10-15, nonspecific s/sxs begin to appear (e.g., malaise, weakness, insomnia, inability to concentrate, N/V)
*oliguria/anuria rare in CKD alone, almost always indicates at least some component of AKI
Cardiovascular Manifestations:
volume overload, edema, systemic HTN
*ischemic heart disease (d/t accelerated atherosclerosis)
*LVH, HF, rhythm disturbances
*uremic pericarditis (pleuritic chest pain)
Skin Manifestations:
*pale (anemia), hyperpigmented (↑ β-MSH production)
*pruritis +/- scratching lesions
*ecchymoses & hematomas (d/t bleeding diathesis)
*uremic frost (i.e., crystallization of urea), uncommon
*skin necrosis (calciphylaxis) & bullous lesions (rare)
Gastrointestinal Manifestations:
*anorexia & N/V (typical of advanced kidney failure)
*malnutrition
*uremic fetor (i.e., urinelike breath odor d/t urea + saliva forming ammonia), often associated w/ metallic taste
*inflammatory/ulcerative lesions & GI bleeding
Neurologic Manifestations:
*CVAs (d/t accelerated atherosclerosis)
*uremic encephalopathy (progressive cognitive impairment leading to seizures & coma if untreated)
*uremic neuropathy (i.e., central, peripheral, & autonomic neuropathy), RLS or burning feet syndrome
Hematologic Manifestations:
*normocytic, normochromic anemia (primarily d/t insufficient EPO production)
*abnormal leukocyte/immune system functions (more frequent & severe infections)
*platelet dysfunction (bleeding, bruising)
Endocrine & Metabolic Manifestations:
*impotence, infertility, ↓ libido (d/t hypogonadism)
*amenorrhea & galactorrhea (d/t hyperprolactinemia)
*insulin resistance + glucose intolerance (azotemic pseudodiabetes), hyperlipidemia
CKD-Mineral & Bone Disorders (CKD-MBD)
Mineral Abnormalities: hyperphosphatemia + hypocalcemia + low vitamin D (calcidiol & calcitriol) lead to secondary hyperparathyroidism (i.e., ↑ bone turnover)
Bone Manifestations (renal osteodystrophy): *all characterized by bone pain & easy fractures
*osteitis fibrosa cystica (brown tumors)
*adynamic bone disease (calcifications), *MC in dialysis pts
*osteomalacia, “soft bones” (growth retardation)
Chronic Kidney Disease & ESKD dx
Initial workup: CBC, CMP, urine dipstick & microscopy, ACR & PCR on random urine sample
*↑ BUN (ref. range 7-20mg/dL)
*↑ creatinine
(ref. range 0.6-1.2mg/dL, female)
(ref. range 0.5-1.1mg/dL, male)
Albumin is the main protein lost through urine in CKD
*Proteinuria is best marker of progression
*anemia (↓ H/H)
*hyperphosphatemia
*hypocalcemia
*hyperkalemia
*metabolic acidosis
*hypermagnesemia
*hyperuricemia
Urinary sediment: +/- broad waxy casts
*result of dilated, hypertrophic nephrons
Evaluation of Metabolic Bone Disease:
*serum calcium, phosphorus, vitamin D, PTH
Other levels to evaluate: Hgb, iron, vitamin B12, folate
IMAGING:
Renal U/S: most useful imaging study, initial TOC
*BL small (<10cm), echogenic kidneys suggest chronic scarring of advanced CKD
*normal/enlarged kidneys can be seen w/ PKD, diabetic nephropathy, HIV-associated nephropathy, plasma cell myeloma, amyloidosis, obstructive uropathy
Doppler ultrasonography: useful if renovascular ischemic disease suspected
Chronic Kidney Disease & ESKD tx
*dietary modifications
*treat reversible causes
*slow progression
*treat complications of kidney failure
*identify patients that will require kidney replacement therapy
Dietary Modifications:
*protein 0.8-1.0g/kg/d
*fiber 20-25g/d
*sodium <2g/d
*potassium 40-70meq/d, avoid NSAIDs
*phosphorous 600-800mg/d
*calcium 1400-1600mg/d
*iron ≥10-18mg/d
BP Control: ACEI/ARBs, diuretics
*goal 125-130/<80
Proteinuria: ACEI/ARBs, SGLT2s
Glucose Control: SGLT2s, GLP-1s
HLD: statins
*TC goal <200mg/dL
*LDL goal <100mg/dL
Volume overload:
*salt restriction + diuretic therapy
Metabolic acidosis:
*bicarbonate supplement
Hyperphosphatemia:
*Non-calcium PO phosphate binders (sevelamer, lanthanum)
Anemia: ESAs
*erythropoietin, darbepoetin alfa
Indications for Nephrologist Referral:
*GFR <30, ACR ≥300, PCR ≥500
*abnormal urine microscopy (cellular casts, non-urologic hematuria, sterile pyuria)
*difficult to manage lab abnormalities
*resistant HTN
*inability to identify a cause
Bladder Carcinoma definition, sx, dx, tx
Transitional cell carcinoma MC type
3x MC in men than women
Risk Factors: smoking
sx
Painless hematuria in a smoker
dx
Cystoscopy w/ bx: gold standard
tx
Endoscopic resection w/ cystoscopy every 3mo
*recurrent or multiple lesions can be treated w/ intravesical chemotherapy
Epididymitis definition, sx, dx, tx
Epididymal pain & swelling thought to be secondary to retrograde infection or reflux of urine – bacterial infection MC
Etiologies:
*males 14-35: chlamydia trachomatis (MC), Neisseria gonorrhea
*men >35: E. coli MC
S/SXS: gradual onset (hours to days) of unilateral testicular pain & swelling
▪︎groin, flank, or abdominal pain
+/- fever/chills, irritative sxs (urgency, frequency, dysuria)
PE:
▪︎scrotal swelling/tenderness
▪︎epididymal tenderness & induration
⊕Prehn sign: relief of pain w/ scrotal elevation
⊕cremasteric reflex: stroking of inner thigh causes elevation of ipsilateral testis
dx
Scrotal U/S – enlarged epididymis, increased testicular blood flow
UA: pyuria (↑ WBCs) or bacteriuria
NAAT for gonorrhea & chlamydia
tx
Scrotal elevation, NSAIDs, cool compresses
<35yrs: doxycycline (100mg BID x10d) + ceftriaxone (250mg IM x1)
> 35yrs: FQs (ciprofloxacin, ofloxacin, levofloxacin)
Hydrocele definition, sx, dx, tx
Serous fluid collection within the layers of the tunica vaginalis of the scrotum
Etiologies: idiopathic MCC
Types:
*Communicating: peritoneal/abdominal fluid enters the scrotum via a patent processus vaginalis that failed to close
*Noncommunicating: derived from fluid from the mesothelial lining of the tunica vaginalis (no connection to the peritoneum)
sx
*painless scrotal swelling
PE:
*translucency (transilluminates)
*fluid located anterior/lateral to the testis
dx: Testicular U/S
tx
Usually no tx needed (watchful waiting)
*often resolves within the first 12mo of life in infants
*often self-limited in adults
Refractory: surgical excision
Varicocele definition, sx, dx, tx
*cystic testicular mass of varicose veins: pampiniform venous plexus & internal spermatic vein
MC surgically correctable cause of male infertility
Most are left sided (increased left renal vein pressure transmitted to left gonadal vein)
sx
Asymptomatic varicocele found in 10% of population
*may cause testicular atrophy
*usually painless but may ⇢ dull ache, heavy sensation
PE:
▪︎“bag of worms” feel superior to testicle
▪︎dilation worsens when pt is upright or w/ Valsalva
dx: clinical
U/S – dilation of pampiniform plexus >2mm
tx
Observation in most
Surgery:
*pain, infertility, delayed testicular growth
ASSOCIATIONS:
*right sided: retroperitoneal/abdominal cancer
*sudden onset left sided in older man: RCC
Testicular Torsion definition, sx, dx, tx
*spermatic cord twists & cuts off testicular blood supply due to congenital malformation
Highest Risk: males 10-20yrs, neonates
PATHO: insufficient fixation of the lower pole of the testis to the tunica vaginalis (Bell-clapper deformity), leading to increased mobility of the testicle
sx
ABRUPT ONSET: scrotal, inguinal, or lower abdominal pain
▪︎N/V
PE:
▪︎swollen, tender, retracted testicle (high-riding), may have horizontal lie
⊖Prehn sign: no pain relief w/ scrotal elevation
⊖cremasteric reflex: no elevation of testicle after stroking the inner thigh
dx
Clinical DX: in pts w/ H&P suggestive of torsion, imaging should NOT be performed **immediate surgical exploration
Emergency surgical exploration (definitive)
▪︎preferred over U/S if torsion is very likely
Testicular Doppler U/S
▪︎decreased or absent testicular blood flow
tx
*urgent detorsion & orchiopexy (ideally within 6hrs of pain onset)
*irreversible damage after 12hrs
*orchiectomy if not salvageable
Erectile Dysfunction (ED) definition, types, sx, dx, tx
Definition: consistent or recurrent inability to generate or maintain an erection
Risk Factors: atherosclerosis (HTN, smoking, hyperlipidemia, diabetes), meds, sickle cell disease, hx of pelvic surgery or perineal trauma, ETOH abuse, hypothyroidism, congenital penile curvature
Medications: beta blockers, thiazide diuretics, spironolactone, CCBs, SSRIs, TCAs
Types
Vascular: MCC!
*atherosclerosis, diabetes, CKD,
Neurologic:
*stroke, seizures, MS, SCI
Psychogenic *abrupt onset
*normal nocturnal erections
*depression, stress
Hormonal:
*GnRH, LH, testosterone
dx
Detailed hx & PE
*DRE
*neuro exam
Labs: CBC, chemistry panel, fasting glucose, lipids
Hormones:
*serum testosterone
*prolactin, thyroid studies
Nocturnal penile tumescence:
*normal erections 🡪 psychogenic cause
Duplex U/S *evaluate penile blood flow
tx
First line: PDE-5 Inhibitors
*Sildenafil, Tadalafil, Vardenafil
Second line: intracavernosal injection therapy
*Prostaglandin E1 (Alprostadil)
*Papaverine +/- Phentolamine
Testosterone replacement therapy
Surgical:
*vacuum pump
*penile prosthesis
*revascularization surgery
Hydronephrosis definition, sx, dx, tx
Water inside kidney 🡪 distention/dilation of pelvis and calyces by obstruction of free flow of urine from kidney
sx
*May be palpable abdominal or flank mass
dx
*Increased BUN/Cr
*Electrolyte imbalance
*IV urogram, US, CT, MRI
tx
*Remove obstruction/drain urine
*Nephrostomy tube: upper tract
*Catheter: lower tract
Renal Cell Carcinoma definition, sx, dx, tx
Tumor of the proximal convoluted renal tubule cells (they are very metabolically active cells so they are the most prone to dysplasia)
95% of primary tumors originating in the kidney
*Clear Cell Carcinoma MC
Characterized by lack of warning signs, variable presentations, & resistance to chemo/radiation
Risk Factors: smoking, HTN, obesity, men, dialysis, cadmium or industrial exposure
sx
Triad:
*hematuria
*flank or abdominal pain
*palpable abdominal mass
*HTN & hypercalcemia
Tumors blocks left testicular vein drainage 🡪 left-sided varicocele
*malaise, weight loss
METS: cannon ball METS to lungs (MC site); bone
dx
CT (initial)
Renal U/S, MRI
Erythrocytosis often present
tx
Stage I-III: radical nephrectomy
*immune-mediated therapy (e.g., interleukin-2 & monoclonal antibody molecular targeted treatment) – usually resistant to radiation/chemo
Bilateral involvement of solitary kidney:
*partial nephrectomy
Advanced disease:
*molecularly targeted agents
*debulking nephrectomy
Renal Artery Stenosis definition, sx, dx, tx
HTN secondary to renal artery stenosis of 1 or both kidneys
*MCC of secondary HTN
PATHO: decreased renal blood flow leads to activation of RAAS
Etiologies:
*atherosclerosis MC in the elderly
*fibromuscular dysplasia MC in women <50yrs
sx
*HA
*<20yrs or >50yrs w/ HTN
*severe HTN
*HTN resistant to 3 or more drugs
PE:
*abdominal bruit
ACEI 🡪 acute kidney injury!!!!!
dx
*CT angiography
*MR angiography
*duplex doppler U/S
Renal catheter arteriography 🡪 GOLD STANDARD*
tx
Definitive 🡪 revascularization
*angioplasty w/ stent
*bypass
Medical: ACEI/ARBs *CI if bilateral stenosis
*thiazide diuretics
*long-acting CCB
*mineralocorticoid receptor antagonist
Nephrolithiasis types, definition, sx, dx, tx
Types:
*calcium oxalate (MC), calcium phosphate
*uric acid: high protein foods, gout, chemo
*struvite: magnesium ammonium phosphate
*cystine: congenital defect in reabsorption
sx
Renal colic: sudden, constant upper lateral back or flank pain over the CVA radiating to the groin or anteriorly; difficult to find a comfortable position
N/V, frequency, urgency, hematuria
PE: CVA tenderness
dx
UA:
*hematuria
*pH <5.0: uric acid, cystine
*pH >7.2: struvite
Non-contrast CT abdomen/pelvis
KUB x-ray: calcium & struvite stones are radiopaque
tx
<5mm:
- 80% chance of spontaneous passage
- IV fluids, analgesics, antiemetics
- tamsulosin
5-10mm:
- 20% chance of spontaneous passage
- extracorporeal shock wave lithotripsy
- ureteroscopy w/ or w/o stent: immediate relief of obstruction
- percutaneous nephrolithotomy: stones >10mm
Osmolality vs osmolarity
Osmolality: dissolved particles per unit mass (mOsm/kg)
Osmolarity: solutes concentration per unit volume (mOsm/L)
Crystalloids vs colloids
Crystalloids: aqueous solutions w/ varying concentrations of electrolytes
*Most commonly used fluids in hospital setting, ⇡ intravascular (ECF) volume
Types: isotonic, hypotonic, hypertonic
Colloids: solutions that contain larger molecular weight solutes (e.g., albumin, starch)
*solutes mostly remain confined to intravascular compartment
*NOT routinely used for fluid resuscitation
Natural Colloids: albumin, FFP
Artificial Colloids: gelatins, dextrans, hydroxyethyl starch (HES)
Volume Depletion (Hypovolemia) definition and causes
HYPOVOLEMIA:
*secondary to loss of sodium AND water from ECF
*results in compromised tissue perfusion
Etiology:
*GI losses: vomiting, diarrhea, bleeding
*Renal losses: diuretics, hypoaldosteronism, osmotic
diuresis via glucosuria, salt-wasting nephropathies
*Skin losses: sweat, burns
*Third-spacing sequestration: intestinal obstruction,
crush injury, ascites, pancreatitis/peritonitis
Compensatory Mechanisms:
*RAAS activation ⇢ Na & H2O reabsorption
*ADH release ⇢ H2O reabsorption
DEHYDRATION:
*H2O loss from ICF ⇢ ECF hypertonicity (⇡ Na)
*H2O net shift: ICF ⇢ ECF
Etiology: insensible losses, diabetes insipidus
S/SXS: secondary to hypernatremia (e.g., HA, confusion, dizziness)
Compensatory Mechanisms:
*activation of thirst center ⇢ increased intake
*ADH release ⇢ H2O reabsorption
Hypovolemia vs dehydration
hypovolemia = Na and H2O loss
dehydration = free water loss
Volume Depletion (Hypovolemia) sx
S/SXS related to VOLUME DEPLETION:
*lack of energy, easy fatigability, thirst, muscle cramps
*postural dizziness, oliguria
S/SXS related to FLUID LOSS ETIOLOGY:
*V/D, polyuria, severe skin burn
*pain caused by underlying third-spacing mechanism
S/SXS related to ELECTROLYTE ABNORMALITIES:
*hyponatremia ⇢ N/V, lethargy, confusion, seizures
*hyperkalemia ⇢ N/V/D, ileus, muscle weakness
*acidosis ⇢ tachypnea
*alkalosis ⇢ neuromuscular irritability (spasms)
Physical Exam:
*⇣ interstitial volume ⇢ skin/mucous membrane signs
▪︎ dry skin, ⇣ turgor, tenting, dry mucous membranes
*⇣ plasma (intravascular) volume ⇢ SBP & JVP reductions
▪︎ SBPΔ as severity of volume deficit increases
⤷ ~NML ⇢ orthostasis ⇢ posture-independent low SBP
▪︎ ⇣ intensity of Korotkoff sounds & radial pulse
▪︎ ⇣ JVP
*Hypovolemic Shock ⇢ tachycardia, cold/clammy extremities, cyanosis, low UO <15mL/h, agitation, confusion
Volume Depletion (Hypovolemia) dx
LABS:
*low urine volume (oliguria)
*BUN/creatinine ratio >20:1
*d/t ⇡ Na reabsorption & resultant ⇣ urea excretion
▪︎ ⇡ BUN (ref. 5-20mg/dL) ⇢ prerenal azotemia
▪︎ creatinine ⇡ only if loss severe enough to ⇣ GFR
*hyponatremia (ref. 135-145mEq/L)
*hyperkalemia (ref. 3.5-5.0mEq/L)
*acid-base disturbances *depends on mechanism of loss
▪︎ vomiting, diuretics (H+ loss) ⇢ metabolic alkalosis
▪︎ diarrhea (HCO3 loss) ⇢ metabolic acidosis
*Hct & albumin *depletion of plasma volume
▪︎ ⇡ Hct (i.e., relative polycythemia)
▪︎ ⇡ albumin (ref. 3.5-5g/dL)
DX: clinical, confirmed by low urine Na concentration
*urine Na <20mEq/L
*FENA <1%
*urine osmolality concentration >450mOsm/kg
▪︎ specific gravity >1.015
*UA normal in hypovolemia since kidney is not diseased
▪︎ i.e., ⊖protein, ⊖cells/casts
Volume Depletion (Hypovolemia) tx
Resuscitation: IV fluid boluses
*20mL/kg IV NS or LR
Maintenance:
*calculate maintenance rate
*D5½NS + 20mEq KCl preferred
Monitor: I&Os, electrolytes, weight
Volume Overload (Hypervolemia) definition, sx, dx, tx
Isotonic Hypervolemia (salt gain = H2O gain):
*intravascular overload of IV fluids w/ electrolytes
*postop/trauma stress causing ⇣ Na/H2O excretion
*renal insufficiency, cirrhosis, CHF
Hypotonic Hypervolemia (salt gain < H2O gain):
*replacement of GI losses w/ NaCl-poor solutions
*third-spacing, ⇡ ADH w/ surgical stress, SIADH
Hypertonic Hypervolemia (salt gain > H2O gain):
*excessive Na load w/o adequate H2O intake
sx
*tachypnea, orthopnea, weight gain
*pulmonary edema, crackles, rales
*ascites, pleural effusions
*⇡ JVD, peripheral edema, oliguria
Hypertonic ⇢ symptoms of sodium excess
*HA, confusion, dizziness, etc.
DX: mainly clinical
*serum Na (ref. 135-145mEq/L)
Supportive labs/imaging:
*CXR, ECHO
*NT-proBNP
tx
*sodium & water restriction
*loop diuretics
*dialysis may be required if severe
Polycystic Kidney Disease definition, sx, dx, tx
Autosomal dominant polycystic kidney disease (ADPKD) is a relatively common genetic condition resulting from mutation of the PKD1/PKD2 gene
Growth of numerous cysts in kidneys made of epithelial cells from renal tubules; can 🡪 kidney failure/ESRD
sx
*>30yrs, + family hx, abdominal mass
Classic presentation 🡪 young pt w/ back/flank pain & HTN
10% have brain aneurysms (worry when they complain of the worse HA of life)
Cardiovascular abnormalities: MVP, LVH
dx
U/S 🡪 many fluid-filled cysts
CT: large renal size; multiple thin-walled cysts
Anemia
UA:
*proteinuria, hematuria
*pyuria, bacteriuria
tx
No cure!!!
BP control – ACEI/ARB for HTN
Treat infections w/ abx
Dialysis/transplant w/ renal insufficiency
Prostate Cancer definition, sx, dx, tx
Adenocarcinoma MC type (95%)
*peripheral zone MC area
Risk Factors: age, family hx, AA
Screening: DRE & PSA level
*white male = 50yrs
*black male, + FH, or +BRCA mutation = 40yrs
sx
*difficulty w/ urination
*frequency, urgency, urinary retention
*decreased urinary stream
DRE:
*hard, indurated, nodular, enlarged, asymmetrical prostate
Back or bone pain 🡪 METS
dx
PSA (normal <4ng/mL), DRE, transrectal U/S
*PSA >10 🡪 transrectal U/S w/ bx
*abnormal DRE 🡪 transrectal U/S w/ bx
*PSA <4, normal DRE 🡪 annual follow-up
*PSA 4-10, normal DRE 🡪 bx recommended
If PSA >10 🡪 order bone scan to r/o METS
Gleason grading system
tx
Radical prostatectomy – complication: ED
w/ METS: androgen deprivation therapy (leuprolide)
Monitor PSA: should be <0.1
Prostatitis definition, sx, dx, tx
Prostate gland inflammation secondary to an ascending infection
Acute:
*>35yrs: E. coli MC
*<35yrs: gonorrhea & chlamydia
Chronic:
*E. coli MC
*proteus
sx
Irritative voiding sxs: frequency, urgency, dysuria
Obstructive sxs: hesitancy, poor or interrupted stream, straining to void, incomplete emptying
Acute: exquisitely tender prostate
*fever, chills, perineal pain
Chronic: nontender (or minimally tender) prostate
*usually presents as recurrent UTIs or intermittent dysfunction
PE: boggy prostate!!!!!
dx
UA & urine culture:
*acute: pyuria & bacteriuria
*chronic: + after massage!
AVOID prostatic massage in acute (may cause bacteremia)
tx
Acute:
>35: FQs or TMP-SMX x4-6wks
<35: ceftriaxone + doxycycline
Chronic: FQs or TMP-SMX x6-12wks
*tamsulosin can help w/ chronic pain
Refractory (chronic): TURP
Acute Cystitis “bladder infection” “UTI”
definition, sx, dx, tx
PATHO: usually an ascending infection of the lower urinary tract from the urethra
Etiologies:
*E. coli MC
*staph saprophyticus 2nd MC in sexually active
sx
Irritative sxs: dysuria (burning), frequency, urgency
*hematuria, suprapubic pain & tenderness
dx
UA: pyuria (>10WBCs/hpf), hematuria, leukocytes esterase, nitrites, cloudy urine, bacteriuria
Urine culture: definitive
*epithelial (squamous cells) = contamination
tx
- nitrofurantoin or TMP-SMX
- FQs second line (“floxacin”)
- phenazopyridine (analgesic)
*turns urine orange
Acute Pyelonephritis “kidney infection” definition, sx, dx, tx
Infection of the upper GU tract (kidney parenchyma & renal pelvis)
PATHO: usually an ascending infection of the lower urinary tract
Etiologies: E. coli MC
Risk Factors: DM, hx of recurrent UTIs or kidney stones, pregnancy, congenital urinary tract malformations
sx
Upper tract sxs: fever, chills, back/flank pain; N/V
Lower tract sxs: dysuria, urgency, frequency
PE:
+ CVA tenderness
Fever, tachycardia
dx
UA:
*pyuria (>10WBCs/hpf)
*leukocyte esterase
*nitrites
*hematuria, cloudy urine
*WBC casts – HALLMARK
CBC: leukocytosis w/ left shift
Urine culture: definitive
tx
Outpatient: FQs first line (“floxacin”)
Inpatient: cephalosporins, FQs, aminoglycosides, penicillins
ADMIT: older age, signs of obstruction, comorbid conditions, inability to tolerate PO abx
Pregnancy: IV ceftriaxone
