Module 8 Outline PDF

I. LITHIASIS Stone Pathogenesis Factors promoting stone formation...

I. LITHIASIS Stone Pathogenesis Factors promoting stone formation - stasis (hydronephrosis, congenital abnormality) NEPHROLITHIASIS & UROLITHIASIS - medullary sponge kidney Etiology: - infection(struvite stones) - Hypercalcemia (Eg. Inc intake, or HyperPTH) > Calcium Stones 80% - Chronic UTI > Triple Phosphate /Struvite/ “Staghorn” Stones 15% - hypercalciuria - Uremia > Urate Stones (+ Gout) - increased oxalate - increased uric acid Pathogenesis: - Hypercalcemia > Calcium in Urine Precipitates out of Solution > Calcium Stones 80% - Chronic UTI > Gram-Neg Rods (Proteus, Pseudomonas & Klebsiella Loss of inhibitory factors - NOT E. coli) > Triple Phosphate/Struvite/ “Staghorn” Stones 15% - magnesium (forms soluble complex with oxalate) - May cause: - citrate (forms soluble complex with calcium) - Urinary Obstruction - pyrophosphate - Hydronephrosis - Stretching of Renal - glycoprotein - Capsule > Pain) Morphology: STONE TYPES a. Calcium Stones (80%) Small, hard Stones (1-3mm); Stones have sharp edges 1. Calcium Stones Radio-Opaque - Account for 80 - 85% of all stones - Ca2+ oxalate most common, followed by Ca2+ phosphate description b. Triple Phosphate/Struvite/ “Staghorn” Stones (15%) - gray or brown due to hemosiderin from bleeding - Large Stones (Molds to Renal Pelvis/Calyces) (Hence Staghorn͘) - radiopaque - Chronic irritation of surrounding epithelium - may lead to squamous metaplasia 2. Struvite Stones Clinical Features: - Female patients affected twice as often as male patients - Usually, Unilateral or Painful Hematuria (Macro/Micro) - Writhing in pain͕ pacing about and unable to lie still͟ - Etiology and Pathogenesis - Hydronephrosis > Stretching of Renal Capsule > Flank Pain & Tenderness. - account for 10% of all stones Stone in Ureteropelvic Junction - contribute to formation of staghorn calculi - Deep flank pain. - consist of triple phosphate (calcium, magnesium, ammonium) - No radiation. - due to infection with urea splitting organisms NH2CONH2 + H2O ––> 2NH3 + - Distension of the Renal Capsule. CO2 Stone in Ureter - Intense - NH4 alkalinizes urine, thus decreasing solubility - Colicky Pain (Loin > Inguinal Region > Testes/Vulva) + N/V. Stone in Ureterovesical Junction - Common Organisms - Leads to Dysuria, Frequency, + Tip of penis pain - Proteus - Klebsiella Complications: - Pseudomonas - Hydronephrosis - Providencia - Post-Renal Failure - S. aureus - Infection (UTI/Pyelonephritis/PerinephricAbscess) - not E. coli Investigations: Treatment - Abdo USS – (Confirm Stone) - Complete stone clearance (ESWL/percutaneous nephrolithotomy) - Abdo XR – (Confirm Calcium Vs RadioLucent Stone) - Acidify urine, dissolve microscopic fragments - UECs – inc. Calcium or inc. Urea - Antibiotics for 6 weeks Management: - Follow up urine cultures - Conservative – (Daily Na-Bicarbonate Tablets to Alkalize Urine > Dissolve Urate Stones) - (ESWL) Extracorporeal Shock-Wave Lithotripsy - (For Calcium Stones) 3. Uric Acid Stones - Surgical – (For All Stones Not Amenable to the above) - Account for 10% of all stones Location of Stones a. calyx - Description and Diagnosis may cause: - orange colored gravel, needle shaped crystals flank discomfort - radiolucent on x-ray recurrent infection - filling defect on IVP persistent hematuria - Radiopaque on CT scan - Visualized with ultrasound may remain asymptomatic for years and not require treatment Etiology b. pelvis - hyperuricosuria (urine pH < 5.5) - tend to cause UPJ obstruction renal pelvis and one or more calyces - secondary to increased uric acid production, or drugs (ASA and probenecid) - Hyperuricemia c. staghorn calculi - Gout - often associated with infection - myeloproliferative disease - infection will not resolve until stone cleared - cytotoxic drugs - may obstruct renal drainage - defect in tubular NH3 synthesis (ammonia trap for H+) d. ureter - dehydration, IBD, colostomy and ileostomy - 5 mm diameter - will pass spontaneously in 75% of patients the three narrowest passage points for upper tract stones Treatment - include: - increase fluid intake UPJ - NaHCO3 (maintain urinary pH no less than 6.5) pelvic brim - Allopurinol UVJ - avoid high protein/purine diet 4. Cystine Stones Clinical Presentation - Autosomal recessive defect in small bowel mucosal absorption and renal tubular - Rapid onset (hours to a day) absorption of dibasic amino acids - General Symptoms: - Seen in children and young adults Lethargic and unwell - Aggressive stone disease Fever Tachycardia - Description: Shaking - hexagonal on urinalysis Chills - yellow, hard nausea and vomiting - radiopaque (ground glass) Myalgias - staghorn or multiple - decreased reabsorption of “COLA” - Marked CVA or flank tenderness; possible abdominal pain on deep palpation - cystine (insoluble in urine); ornithine, lysine, arginine (soluble in urine) - Symptoms of lower UTI may be absent (urgency, frequency, dysuria) - May have symptoms of Gram-negative sepsis Diagnosis - amino acid chromatography of urine ––> see COLA in urine Laboratory Investigations - serum cystine - Urine dipstick: +ve for leukocytes and nitrites, possible hematuria - Na+ nitroprusside test - Microscopy: >5 WBC/HPF in unspun urine Treatment > 10 WBC/HPF in spun urine, bacteria ○ greatly increase water intake ––> 3-4 L urine/day - Gram stain: Gram negative rods, Gram positive cocci ○ Bicarbonate (HCO₃⁻) - Culture: ○ decrease dietary protein ––> methionine > 105 colony forming units (CFU)/mL in clean catch midstream urine ○ penicillamine chelators ––> 2 g daily, soluble complex formed; use cautiously > 102 CFU/mL in suprapubic aspirate or catheterized specimen ○ a-mercaptopropionylglycine (MPG) ––> similar action to penicillamine, less toxic - CBC and differential: ○ captopril (binds cysteine) ○ Irrigating solutions: Leukocytosis N-acetylcysteine (binds cystine) high % neutrophils Tromethamine-E left-shift (increase in band cells - immature neutrophils) - Blood cultures: may be positive in 20% of cases, especially in S. aureus infection II. COMMON INFECTIONS OF THE URINARY SYSTEM - Consider investigation of complicated pyelonephritis: if fever, pain, leukocytosis not resolving with treatment within 72 hr, if male patient, or if there is history of urinary tract abnormalities a. Pyelonephritis Additional Tests: - abdominal/pelvic ultrasound 1. Acute Pyelonephritis - CT for renal abscess, - Infection of the renal parenchyma with local and systemic manifestations of infection - spiral CT for stones, cystoscopy) - may be classified as uncomplicated or complicated Treatment uncomplicated: - Uncomplicated pyelonephritis with mild symptoms in the absence of conditions predisposing to anatomic or functional impairment 14-day course of TMP/SMX or fluoroquinolone or third generation cephalosporin of urine flow Start with IV for several days and then switch to PO (can then be treated as outpatient) complicated: occurring in the setting of: - Renal Or Ureteric Stones - Patient more than mildly symptomatic or complicated pyelonephritis in the setting of stone - Strictures obstruction is a urologic emergency (placing patient at risk of kidney loss or septic shock) - Prostatic Obstruction (Hypertrophy Or Malignancy) start broad spectrum IV antibiotics until cultures return (imipenem or - Vesicoureteric Reflux meropenem or piperacillin /tazobactam or ampicillin plus gentamicin) and - Neurogenic Bladder treat 2-3 weeks - Catheters - Dm - If No Improvement in 48-72 Hours: - Sickle-Cell Hemoglobinopathies need to continue on IV antibiotics, - Polycystic Kidney Disease assess for: - Immunosuppression - complicated pyelonephritis - Post-Renal Transplant - possible renal or perinephric abscess Etiology Prognosis - Usually ascending microorganisms, most often bacteria - Treated acute pyelonephritis rarely progresses to chronic renal disease - in females with uncomplicated pyelonephritis usually E. coli - Recurrent infections often constitute relapse rather then re-infection - causative microorganisms are usually: - E. coli, Klebsiella 2. Chronic Pyelonephritis - Proteus, Serratia - A form of chronic tubulointerstitial nephritis of bacterial origin - Pseudomonas - Cortical scarring, tubulointerstitial damage, and calyceal deformities seen - Enterococcus - S. aureus - May be: - If S. aureus is found, suspect bacteremic spread from a distant focus (e.g. septic emboli in active (persistent infection) infective endocarditis) and suspect (possible multiple intra-renal micro abscesses or inactive (persistent focal sterile scars postinfection) perinephric abscess) - Histologically indistinguishable from many other forms of TIN: severe vesicoureteral reflux hypertensive disease analgesic nephropathy - Active chronic pyelonephritis may respond to antibiotics - Need to rule out TB III. GLOMERULAR DISEASES b. NEPHRITIC SYNDROMES (Complete Glomerular-Membrane Damage) Clinical Features of Nephritic Syndrome: a. NEPHROTIC SYNDROMES - Dec GFR (Incomplete Glomerular-Membrane Damage) - Oliguria Renal Hypertension: (Hypoperfusion of JG Cells due to dec GFR) Fluid Overload Edema: (dec Plasma Osmolality & Na + H2O Retention) Clinical Features - Microalbuminuria Normal GFR - Hematuria++++ +++Polyuria RBC (Cellular) Casts. ++++ Proteinuria (>3000mg/day: Nephrotic) Anemia - o > Granular (Protein) Casts. - Inc. Creatinine - o > Edema (Especially Periorbital) - o > Hypercoagulability (Loss of Antithrombin-III in Urine) NOTE: Fluid Overloaded due to Oliguria; And Edematous due to Fluid Overload) - > Immunocompromised state (Loss of Ig in Urine) - Hyperlipidemia (Attempted Hepatic Compensation for dec. Plasma 1. PSGN (Post-Strep Glomerulonephritis) Osmolarity) - PSGN = THE Childhood cause of Nephritic Syndrome (3-15yrs) Serum Creatinine Mildly Elevated - Eg. 8-year-old girl with fever, oliguria, smoke colored urine & hypertension following upper - (Dehydrated due to Polyuria; But Edematous due to Proteinuria) respiratory tract infection. 1. MCD (Minimal Change Disease) / Foot Process Disease/ Nil Disease) Etiology: - THE Childhood cause of Nephrotic Syndrome (1-8yrs) - Post-Infective (GABH-Streptococcal Pharyngitis) Ag:Ab Complex Deposition Etiology: Post-Infective (usually after URTI) Clinical Features: Clinical Features: - Nephritic Syndrome - Eg. 2yo Boy with sudden onset Polyuria, Oedema & Proteinuria following URTI. Oliguria - Children (1-8yrs) Painless Hematuria Non-Selective Proteinuria Prognosis Edema - Spontaneous Remission 50% of Adult Nephrotic Syndrome: Etiology 2. IgA Nephropathy (Berger’s Disease) - Autoimmune - Ag:Ab Complex Deposition - THE Adult (15-30yrs) - Eg. 18y male Recurrent, Episodic Painless Hematuria, 3-6 days, usually following URTI. Clinical Features: - Eg. 35y female, Tired for years, Worsened for two months. Etiology: - She has noted swelling of her legs and puffiness around eyelids - Autoimmune: Ag IgA Complex Deposition in Glomerulus - (Periorbital edema - A classic sign of nephrotic syndrome). - Adults - 40-60yrs Clinical Features: - Nephrotic Syndrome - Polyuria, +++ Proteinuria, edema. - Nephritic Syndrome Oliguria Prognosis Painless Hematuria - Good, but Occasionally progresses to ESRD Non-Selective Proteinuria Edema 3. FSGS (Focal Segmental Glomerulosclerosis) Hypertension - Slowly Progressive - Often a recent history of an URTI - 10% > Renal Failure Clinical Features: 3. RPGN (Rapidly Progressive Glomerulonephritis): - Eg., 49 y/o Nephrotic Syndrome, non responsive - NOT a Separate Disease - Nephrotic Syndrome - +++ Selective Proteinuria - ANY Glomerulonephritis can > RPGN Etiology: Prognosis: Poor: - Progression of any Glomerulonephritis (Autoimmune) - 30% Remission - 50% CKD Pathogenesis: - 20% RPGN - Rapidly Progressing Glomerulonephritis > Renal Failure within Weeks. Clinical Features: - Nephritic Syndrome Oliguria Painless Hematuria Non-Selective Proteinuria Oedema Hypertension Prognosis: - Poor: Quickly progresses to ESRF IV. RENAL FAILURES Investigations: Blood Urea to Creatinine Ratio a. Acute Renal Failures ★ Decreased U Acute Renal Failure - General Information: - Indicates Intrarenal Failure (suggesting kidney pathology) Etiology: - Causes: Infection, toxins, ischemia, or hypoxia - Rapid loss of kidney function ★ Increased U 1. Prerenal Renal Failure: - Can indicate Pre-renal or Post-renal Failure (with normally functioning kidneys) - Before the Blood Reaches the Kidney (Ie. Dec. Glomerular Perfusion) Pre-renal causes: Hypotension, dehydration Hypovolemia (Eg. Blood Loss) Post-renal causes: BPH, bladder stone Decreased cardiac output (Eg. Heart Failure) Renal artery obstruction (Eg. Embolism) Urine Protein: Creatinine Ratio - Is there Proteinuria? 2. Intrarenal Renal Failure Interpretation: - The kidney itself is damaged - Daily Creatinine Excretion is Constant Acute glomerulonephritis - inc P: CR = Inc Protein in Urine = Proteinuria Tubular diseases (e.g., acute tubular necrosis) 30-300 mg = Microalbuminuria Interstitial diseases (e.g., autoimmune disorders such as SLE) >300mg = Macroalbuminuria/Proteinuria͘ Vascular diseases (e.g., polyarteritis nodosa) >3000mg = Nephrotic Syndrome 3. Post-Renal Renal Failure - Due to outflow obstruction from the kidneys b. Chronic Renal Failure Cancer - Bladder / Prostate / Ureteric / Cervical Blood clot General Information: Calculi (Kidney stones - Bilateral) - Many etiologies: continuum of progressive nephron loss and declining renal function Accidental surgical ligation - Asymptomatic until severe insufficiency develops - Regional variation in leading causes worldwide Clinical Features: In North America: Uremia - diabetes (> 30%) - Fatigue - hypertensive renal disease (23%) - Malaise - chronic GN (10%) (e.g. IgA nephropathy), - Anorexia - polycystic kidney disease (5%) - Headache - Nausea - Frequently patients present at end-stage with small, contracted kidneys, - Vomiting unknown etiology Hyperkalemia - Leads to Brady-Arrhythmias Classification Fluid Retention - glomerular: primary or secondary glomerulonephritis - Oedema (Peripheral Pulmonary) - tubulointerstitial disease (e.g., autoimmune interstitial nephritis) - RARELY, Hypertension & Cardiac Tamponade. - vascular (e.g., DM, HTN) Hematuria - hereditary (e.g. autosomal dominant polycystic kidney disease, Alport’s) - Often indicates Painless (Cancer) - Suggests Painful (Stones/LUTS) INDICATIONS FOR DIALYSIS IN CRF Flank pain (in specific conditions) - Maybe same as ARF - Particularly Inflammatory or Ischemic) - more commonly = “dwindles” ★ Symptoms: 4 Stages of Chronic Renal Failure Anorexia 1. Stage 1 = > 90 ml/min GFR (Normal) plus other signs of renal disease Nausea 2. Stage 2 = 90-60 ml/min GFR Vomiting 3. Stage 3 = 60-30 ml/min GFR Severe fatigue 4. Stage 4 = 30-15 ml/min GFR Pruritus 5. Stage 5 = Na+ & K+ Retention) Fluid Balance (Renal Failure > Fluid Overload) Dec Erythropoiesis (Renal Failure > Anemia) Renin Angiotensin System > Renal Hypertension Calcium Metabolism (Renal Failure > Osteoporosis & secondary HPT) Uremia Dec Urine Output Dec Toxin Excretion (Renal Failure > Accumulation of Urea & Creatinine)