Uro/Renal Flashcards
(46 cards)
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