Cola-colored urine Flashcards

Question

Findings of HSP Nephritis in light microscopy, IF and EM

Answer 1

Light microscopy: Leukocytoclastic vasculitis/angiitis with IgA C3, and fibrin deposition IF: Deposition of polymeric IgA in the glomeruli EM: Mesangial deposits

Answer 2

1. UA - Done weekly during active ds then once monthly for 6 mos (if all N, GN unlikely) 2. Mild: resolves spontaneously 3. Moderate to severe ds: a. CS (prednisone 1mkd x 3 mos) b. ACEI c. Followed by azathioprine or mycophenolate if persistent 4. Refer to nephro – if with proteinuria, renal insufficiency, HTN 5. Adequate hydration, bland diet 6. Pain control with Pct

Answer 3

Prognosis 2-5% risk of CKD Older children and adolescents have more severe ds Majority do not have severe renal ds/ serious sequelae

Answer 4

HEMOLYTIC UREMIC SYNDROME (HUS) - One of the MC cause of ARF in young children - Usually preschool and school-aged children, MC <4yo Etiology - MC form due to Shiga toxin-producing E.coli 0157:H7 (STEC) - SLE, HELLP syndrome, genetics, drugs (calcineurin inhibitors, cytotoxic agents, clopidogrel, ticlopidine, quinine) Patho - Toxin initiates endothelial cell injury which leads to microvascular injury - Microangiopathic anemia due to mechanical damage to RBCs as they pass through the altered vasculature - Thrombocytopenia due to intra-renal platelet adhesion or damage

Answer 5

Triad a. Microangiopathic hemolytic anemia b. Thrombocytopenia c. Renal insufficiency

Answer 6

1. Triad a. Microangiopathic hemolytic anemia b. Thrombocytopenia c. Renal insufficiency 2. Hx of bloody AGE within the preceding 3 weeks 3. Sudden onset of pallor, irritability, weakness, lethargy, oliguria 4. Usually 5-10d after initial illness 5. Dehydration, petechiae, hepatosplenomegaly, marked irritability 6. CV: HTN, pericarditis, myocardial dysfunction, arrythmia 7. E’ abN – hyperK, hypoNa 8. CNS – encephalopathy, sz 9. GI – inflammatory colitis, ischemic enteritis, bowel perforation, intussusception, bleeding

Answer 7

The following re both present at some time during the illness: 1. Anemia (acute onset) with microangiopathic changes (schistocytes, burr cells, helmet cells) on PBS 2. Acute renal injury: hematuria, proteinuria, elevated creatinine levels (>1.5 mg/dL in >13 years old or ≥50% increase over baseline

Answer 8

-----PROBABLE----- meets lab criteria but with no clear history of diarrhea in the preceedig 3 weeks or onset within 3 weeks of diarrhea, and meets the lab criteria except that microangiopathic changes are not confirmed -----CONFIRMED----- meets the laboratory criteria AND began within 3 weeks of diarrhea

Answer 9

1. PBS – microangiopathic hemolytic anemia, Helmet cells, burr cells, fragmented RBCs 2. CBC – anemia, thrombocytopenia (20K-100K), leukocytosis 3. Inc reticulocyte count 4. (-)Coomb’s test 5. Elevated BUN and crea, ARF 6. UA – hematuria, proteinuria 7. N PT and PTT 8. Stool C/S – negative usually 9. Renal biopsy – glomerular thickening of capillary walls, narrowing of capillary lumen, plt-fibrin thrombi in glomerular capillaries, thrombi in afferent arterioles with fibrinoid necrosis

Answer 10

Mgt 1. Supportive tx and hydration 2. PRBC transfusion 3. Correction of e’ abN 4. Control of HTN 5. Dialysis 6. Plt transfusion – generally not done 7. No Abx – may precipitate toxin release

Answer 11

RAPIDLY PROGRESSIVE (CRESCENTIC) GLOMERULONEPHRITIS (RPGN) CM 1. Acute nephritis with proteinuria or nephrotic syndrome 2. Rapid loss of renal function – deterioration within 3 weeks to 3 mos 3. Renal failure/ insufficiency 4. Primary or secondary to other conditions (IgA nephropathy, HSP nephritis, PSGN, SLE) 5. Most often idiopathic

Answer 12

Dx 1. ID cause of RPGN 2. Crescent = ominous sign, poor prognosis Light microscopy: Crescents in 50% or more in the glomeruli IF: No immune deposits. ID underlying cause EM: No deposits 3. Renal biopsy – indications a. ARF b. Nephrotic syndrome that is persistently hypertensive c. C3 will not normalize in 6-8 weeks in nephritic syndrome d. High suspicion that it is secondary GN that is not post-infectious or MCD e. Steroid-resistant, relapsing requiring medications other than steroids

Answer 13

Mgt 1. High-dose CS 2. Cyclophosphamide 3. ESRD in most pxs 4. Guarded prognosis High-dose CS 2. Cyclophosphamide 3. ESRD in most pxs 4. Guarded prognosis 5. Always refer if secondary GN because multispecialty mgt needed

Answer 14

CH 527: NEPHROTIC SYNDROME (NS) - Suspect when there is nephrotic range proteinuria (>3.5 g/d or UPCR >2) PLUS the clinical triad of nephrotic syndrome: o Hypoalbuminemia (<2.5g/dl) o Edema o Hyperlipidemia (cholesterol >200mg/dl) - “EPAL”: Edema, Proteinuria, Albuminemia (hypo), Lipidemia (hyper)

Answer 15

Approach to edema: Where did the edema 1st manifest? Face going down - renal bipedal edema going up - cardiac central - liver others – nutritional

Answer 16

Etiopatho - M>F - MCD NS: MC in children (90%) - Non-MCD (10%): FSGS, MPGN, C3 GN, MN - Most respond to steroids - Among those nonresponsive to CS, 80% would be FSGS - Ongoing inflammation affects the physical barrier à wider podocyte spaces/ effacement and abnormal charge of barrier (- to +) à protein leakiness across glomerular capillary wall into urinary space

Answer 17

CM Hallmarks of NS: 1. Heavy proteinuria (40mg/m2/h) – due to inc permeability of the glomerular capillary wall 2. Hypoalbuminemia (<2.5g/dl) – due to urinary protein loss 3. Edema - Underfill hypothesis: proteinuria leads to a decrease in plasm protein and low intravascular oncotic P, resulting in leakage of plasma water into interstitium, leading to edema - Overfill hypothesis: NS is associated with urinary sodium retention leading to volume expansion and leakage of excess fluid into the interstitium - Reduced intravascular volume result to increased vasopressin and Atrial natriuretic factor and aldosterone, which result to inc Na and water retention by the tubules 4. Hyperlipidemia – low albumin stimulates generalized hepatic protein synthesis - Increased urinary loss of lipoprotein lipase causes decreased lipid catabolism this elevating serum lipid levels 5. Others: a. Anorexia, irritability, abdominal pain b. HTN, gross hematuria (uncommon)

Answer 18

Types 10% have secondary NS 90% have idiopathic NS: 1. Minimal change disease (85%): 95% respond to CS 2. FSGS (10%): only 20% respond to CS 3. Mesangial proliferation (5%): 50% respond to CS

Answer 19

-----1. Urine Disptick Test----- Routine screening in selected population Interpretation: Normal should be negative or trace if specific gravity (SG ≥1.020; nephrotic range usually +3 or +4; dipstick interpretation: Trace 10-29 mg/dl 1+: 3-100mg/dl 2+: 100-300mg/dl 3+: 300-1000mg/dl 4+: >1000mg/dl Normal SG: 1.015-1.025 Remarks: False-positive: Alkaline urine PH>7.0 or very concentrated urine (SG>1.025); presence of blood, pyuria, prolonged dipstick immersion False negative: low urine pH (<4.5);; dilute urine, if albumin is not the urinary protein -----2. 24-hr Urine Protein and Creatinine Excretion----- Quantitation of proteinuria Normal: <100mg/m2/24h or <150mg/24hr Nephrotic range: 3.5g/24hr or >40 mg/m2/hr Remarks: more accurate -----3. Spot urine for Protein/creatinine Ratio (UPCR)----- semiquantitative assessment of proteinuria Normal: <0.2mg protein/mg creatinine in >2yrs old <0.5 mg protein/mg creatinine in 6-24 mos nephrotic range: >2mg protein/mg creatinine Remarks: easier collection; use first morning void, less accurate than 24hr urine collection; not readily available -----4. microalbuminuria----- Assess risk of progressive glomerulopathy Normal: <30mg of urine albumin per gram of creatinine on first morning void

Answer 20

1. UA – 3+ to 4+ proteinuria - Significant proteinuria = trace with sp gr <0.010 or >1+ with sp gr >0.015 2. Urine protein - >40 mg/m2/h - 24 hr urine collection: 4-40= abnormal 3. Urine protein-creatinine ratio (UPCR) >2 - NV = <0.5 in children <2yo <0.2 in >2yo - Spot urine crea total protein: >2 = nephrotic range 0.2-2 = abnormal protein excretion <0.2 = normal 4. N serum crea, BUN 5. Serum albumin <2.5 g/dl - NV = 2.5-3.5 6. Elevated serum cholesterol & TG 7. N C3 and C4 8. Renal biopsy – indications: a. Gross hematuria b. HTN c. Renal insufficiency d. Hypocomplementenemia e. Age <1 yo or >12 yo

Answer 21

Mgt 1. CS – if onset 1-8yo: likely steroid-responsive MCD (CS may be initiated w/o biopsy) - Prednisone 60mg/m2/d or 2mkd (max 60mg daily) for 4-6 weeks - IF (-) proteinuria: Taper prednisone after 4 weeks to alternate day tx (starting at 40mg/m2/d or 1.5mkd) for 4 weeks then taper gradually over 4 weeks - 12 weeks total duration

Answer 22

remission attained during first 4 weeks of steroid therapye

Answer 23

UPCR <0.2 or dipstick <1 for 3 consecutive days

Answer 24

UPCR >2 or dipstick ≥3+ for 3 consecutive daysS

Answer 25

two consecutive relapses during corticosteroid therapy or within 14 days of ceasing therapy

Answer 26

Failure to achieve complete remission after 8 weeks of steroid therapy; requires renal biopsy and referral to specialist

Answer 27

>2 relapses within 6 mos of initial response or >4 relapses within 12 mos

Answer 28

2. Admission/OPD - OPD: 1st episode w/ mild-mod edema - Admit: severe sx’c edema (effusion, ascites) - r/o TB prior to CS tx 3. fluid balance – fluid restriction and low sodium diet 4. diuretics – furosemide 1mkdose IV 5. IV 25% human albumin 0.5 g/kg for 2-4hrs with postinfusion of furosemide daily - For massive/sx’c pleural effusions (dyspnea), ascites, scrotal/labial edema (difficulty ambulating), oliguria - Temporary relief 6. Monitor volume status, serum e’s, renal fxn 7. Vaccination – pneumococcal vaccine when in remission and off daily CS - varicella vaccine when prednisone <1mkd daily or 2mg/kg on alternate days - Influenza vaccine 8. Treat concurrent infection with abx – 3rd gen ceph 9. Steroid-sparing – Tacrolimus, cyclophosphamide

Answer 29

Complications 1. Infection – major complication (spontaneous bacterial peritonitis (SBP), bacteremia) - S.pneumonia (MC in children) and E.coli - Peritoneal leukocyte count >250 cells/uL highly suggestive of SBP 2. Hypovolemia 3. Thrombosis – do preventive ambulation 4. Malnutrition 5. Acute renal failure

Answer 30

Prognosis - If steroid-resistant: FSGS is usual form with poorer prognosis - In remission: pxs are considered N and may have unrestricted diet and activity

Answer 31

CH 547: UROLITHIASIS - 90% calcium - 60% Ca oxalate - Cystine, UA, indinavir, melamine - RF: low urine volume, low urine pH (acidic), Ca, Na, oxalate, urate - Ca stones – ketogenic diet, CS, VitD - Struvite stone – UTI, FB, urine stasis - When urine contains more crystal-forming substances (Ca, oxalate, uric acid) --> kidney stone formation in renal parenchyma or renal collecting system --> pass to ureter/ bladder --> calculi may lodge in the ureter causing hydroureter/hydronephrosis

Answer 32

CM 1. Severe flank pain (renal colic), intermittent at ureteropelvic junction (narrowest segment) 2. Dysuria, urgency, frequency (distal ureter) 3. Asx’c – if at bladder

Answer 33

Dx 1. PFA – radiopaque stones (ca oxalate/PO4, struvite), radiolucent (urica acid, cystine) 2. Unenhanced spinal CT scan of abdomen, pelvis – most accurate. Opaque stones 3. Renal UTZ – echogenic foci, acoustic shadowing , twinkle artifact on color doppler

Answer 34

Mgt 1. Alpha-adrenergic bladder – Tamsolusin, Terazosin, Doxazosin: decrease P and peristaltic contractions 2. Ureteral stent 3. Lithotripsy (ESWL) – for large proximal calculi - Indication for surgical mgt: a. Stones >5mm b. Extended duration of sx c. Location of the stone with proximal calculi less likely to spontaneously pass d. Infection/sepsis e. Pilot/truck driver due to risk of renal calculi during work f. Solitary kidney g. Failed conservative mgt 4. Diet – dec Na, oxalate, inc hydration 5. Alkalinization of urine

Answer 35

CH ?: RENAL TB Refer to TB (p.36) CM 1. Dysuria, hematuria, flank pain 2. Albuminuria, proteinuria, sterile pyuria

Answer 36

CH 529: RENAL TUBULAR ACIDOSIS (RTA) - Characterized by normal anion gap hyperchloremic metabolic acidosis in the setting of normal or nearnormal GFR

Answer 37

*Inherited and persistent from birth or occur transiently during infancy *Usually occurs as a component of global proximal tubular dysfunction (Fanconi syndrome: proteinuria, glycosuria, phosphaturia, aminoaciduria and proximal RTA) CM: growth failure in the 1st year of life, polyuria, hyponatremic dehydration, anorexia, vomiting, constipation, hypotonia, hypokalemia

Answer 38

*sporadic or inherited *can occur as a complication of inherited or acquired diseases of the distal tubules *results from impaired H+ ion excretion so urine pH cannot be reduced to <5.5 CM: growth failure, hypokalemia, nephrocalcinosis, and hypercalciuria Absent phosphate and bicarbonate wasting

Answer 39

*due to impaired aldosterone production (hypoaldosteronism) or impared renal responsiveness to aldosterone (pseudohypoaldosteronism) *Aldosterone has a direct effect on hydrogen secretion and stimulates K+ secretion in the collecting tubules *lack of aldosterone results in acidosis and hyperkalemia CM: growth failure, hyperkalemia polyuria and dehydration from salt wasting are common urine may be alkaline or acidic high urinary sodium levels with inappropriately low urinary K+

Answer 40

*very rare, autosomal recessive *due to inherited carbonic anhydrase 2 deficiency *features of both proximal and distal RTA CM: associated with osteopetrosis or marble stone disease, cerebral calcification and mental retardation CM: growth failure, bone fractures, facial dysmorphism, conductive hearing loss and blindness

Answer 41

-----PROXIMAL RTA----- urine pH with acidosis: <5.5 urine net charge: negative Fanconi lesions: present Fractional bicarbonate excretion: >10-15% during alkali therapy responsive to therapy: least responsive associated disease: Fanconi syndrome -----CLASSIC DISTAL RTA----- urine pH with acidosis: >5.5 urine net charge: positive Fanconi lesions: absent Fractional bicarbonate excretion: 2-5% responsive to therapy: responsive associated disease: Nephrocalcinosis -----GENERALIZED DISTAL DYSFUNCTION----- urine pH with acidosis: <5.5 to >5.5 urine net charge: positive Fanconi lesions: absent Fractional bicarbonate excretion: 5-10% responsive to therapy: less responsive associated disease: Renal insufficiency 1. E’s, ABG, BUN, Crea, UA

Answer 42

Mgt 1. Bicarbonate replacement – mainstay of tx in all forms of RTA a. Proximal RTA – bicarbonate up to 20 mEq/k/d (sodium bicarbonate or sodium citrate solution) b. Distal RTA – base requirement is generally 2-4 mEq/k/d and required monitoring for the devt of hypercalciuria. i. Thiazides – for sx’c hypercalciuria, nephrocalcinosis, or nephrolithiasis to decrease urine Ca excretion 2. Phosphate supplementation – for Fanconi syndrome 3. Sodium-potassium exchange resin – for type IV RTA as chronic tx for hyperkalemia Prognosis - Depends on nature of existing underlying disorder - Isolated RTA generally show improvement in growth if bicarbonate levels are within N range

Answer 43

CH 535: ACUTE AND CHRONIC RENAL FAILURE ACUTE KIDNEY INJURY - Abrupt loss of kidney function, which leads to rapid decline in the GFR, accumulation of waste products, and dysregulation of extracellular volume and electrolyte homeostasis CM 1. Prerenal AKI – tachycardia, dry mucus membranes, poor perfusion 2. Intrinsic AKI – HTN, peripheral edema, rales, cardiac gallop suggesting volume overload 3. Rash, arthritis - rheuma

Answer 44

1. CBC – anemia (dilutional/hemolytic), leukopenia, thrombocytopenia 2. E’ – hypoNa, hyperK, hyperP, hypoCa 3. ABG – metabolic acidosis 4. Elev BUN, Crea 5. Elev uric acid 6. UA – hematuria, proteinuria, (+)RBC casts, granular casts = GN/ATN vs. WBC/WBC casts = tubuloint. Ds

Answer 45

-----RISK----- Crea: increase >1.5x eGFR: decreased by 25% UO: <0.5ml/kg/hr for ≥8 hours -----INJURY----- Crea: Increase ≥2x eGFR: decreased by ≥50% UO: <0.5ml/kg/hr for ≥16 hours ------FAILURE----- Crea: increase ≥3x or >4 mg/dl with an acute rise of 0.5 mg/dl eGFR: decreased by ≥75% or <35ml/min/1.73m2 UO: <0.3ml/kg/hr for ≥24 hours or anuria for ≥12 hours -----LOSS----- persistent failure > 4weeks -----End-stage----- persistent failure > 3 months

Answer 46

-----PRERENAL----- decreased effective circulating arterial volume leading to inadequate perfusion and decreased GFR dehydration, AGE, burns, sepsis, hemorrhage, capillary leak hypoalbuminemia cardiac failure anaphylaxis cirrhosis abdominal compartment syndrome -----INTRINSIC RENAL------ renal parenchymal damage with sustained hypoperfusion and ischemia Glomerulonephritis HUS ATN Renal vein thrombosis Acute interstitial nephritis Rhabdomyolysis tumor infiltration drugs and toxins Tumor lysis syndrome vasculitis cortical necrosis -----POSTRENAL----- obstruction of the urinary tract posterior urethral valves urolithiasis tumors ureteropelvic and ureterovesicular junction obstruction urethral strictures hemorrhagic cystitis neurogenic bladder anticholinergic drugs

Answer 47

results: Pre-renal AKI Intrinsic AKI Sp gravity >1.020 <1.010 UOsm >500 mOsm/kg <350 Una <20 mEq/L >40 Fractional excretion of Na <1% (<2.5% in NB) >2% (>10% in NB)

Answer 48

Mgt 1. bladder catheter – to ensure adequate drainage of urinary tract 2. IVF - isotonic saline 20ml/kg for 30min for volume resuscitation - Prerenal AKI voids within 2hrs 3. After resuscitation, furosemide (2-4mg/kg) and mannitol (0.5 g/kg) + dopamine (2-3 ug/kg/min) to increase renal cortical blood flow 4. Correct e’ abN a. hyperK – ECG monitoring, Kayexalate b. hypoCa – Ca carbonate/acetate, low P diet c. hypoNa – hypertonic 3% NSS 5. Ranitidine – for GI bleed 6. BP control – diuretic 7. Sz control – BZD 8. Anemia - PRBC 9. Diet – restrict Na, K, and Phosphorus. 10. Dialysis

Answer 49

Indications for Dialysis in AKI: 1. Anuria/ oliguria 2. Volume overload with HTN/ pulmonary edema refractory to diuretics 3. Persistent hyperkalemia 4. Severe metabolic acidosis unresponsive to therapy 5. Uremia (encephalopathy, pericarditis, neuropathy) 6. BUN >100-150 mg/dl (or lower if rapidly rising) 7. Ca:Phosphorus imbalance, with tetany that cannot be controlled 8. Inability to provide adequate nutrition due to severe fluid restriction

Answer 50

CHRONIC KIDNEY DISEASE (CKD) Criteria for definition of CKD: 1. Kidney damage for >3 months - Structural or functional abnormalities of the kidney, with or without decreased GFR, manifested by >1 of the ff: a. abN composition of blood or urine b. abN imaging tests c. abN kidney biopsy 2. GFR <60 ml/min/1.73m2 for >3 months, with or without the other signs of kidney damage described above

Answer 51

STAGE 1: Kidney damage with normal or increased GFR GFR (ml/min/1.73m2): >90 STAGE 2: Kidney damage with mild decrease in GFR GFR (ml/min/1.73m2): 60-89 STAGE 3: moderate decrease in GFR GFR (ml/min/1.73m2): 20-59 STAGE 4: severe decrease in GFR GFR (ml/min/1.73m2): 5-29 STAGE 5: Kidney Failure GFR (ml/min/1.73m2): <15 or on dialysis

Answer 52

CM 1. Edema, HTN, hematuria, proteinuria 2. FTT, polyuria, dehydration, overt renal insufficiency 3. Headache, fatigue, lethargy, anorexia, vomiting, polydipsia, polyuria, growth failure 4. Pallor, sallow appearance, short stature, edema, fluid overload

Answer 53

Dx 1. CBC – normochromic normocytic anemia 2. Elevated BUN, Crea 3. E’ abN – hyperK, hypo/hyperNa, acidosis, hypoCa, hyperP, elev uric acid 4. Hypoalbuminemia 5. Elevated cholesterol and TG 6. UA – hematuria, proteinuria

Answer 54

Mgt 1. Monitoring - Routine serum e’s, BUN, Crea, Ca, P, albumin, ALP, CBC, echo (r/o cardiac complication) 2. Refer to nutritionist/GI 3. Vit D therapy (calcitriol) – cornerstone of tx for renal osteodystrophy - Due to secondary hyperparathyroidism (monitor PTH) - Muscle weakness, bone pain, fractures with minor trauma 4. Fluid and e’ mgt – high volume low caloric density feedings 5. Mgt of HTN – thiazide diuretics à ACEI, ARBs