Nephrology Flashcards
At least 5 RBC/mcl of urine
Hematuria
Abnormal amount of protein in urine
>1 +
Proteinuria
<0.5 ml/kg/hr in children
<0.1 ml/kg/he in infants
Oliguria
> 5 ml/kg/hr, >2L/day
Polyuria
> 5 WBC/hpf
Pyuria
5 year old
2 day history of facial edema, bipedal edema
cola colored urine
multiple dried skin lesions
BP=150/90
PSGN
Most common glomerular cause of hematuria in children
Post Strep Glomerulonephritis
GABHS infection of throat or skin
Mediated by immune complex Type III on the glomeruli
Lumpy bumpy appearance
Complex leads to Inflammatory cascade and leads to hematuria
Sodium and water retention -> inc BP
Post Strep Glomerulonephritis
Acutr NEPHRITIC syndrome
Sudden onset gross or microscopic hematuria
Edema
HTN
Oliguria/renal insuffiency
PSGN
Onset of PSGN occurs 1-6 weeks after infection
comes from
marker
Strep throat infection
ASO titer
Onset of PSGN occurs 3-6 weeks after infection
Comes from
marker
Pyoderma
Anti-DNAse B:
Persistent microscopic hematuria in PSGN persists up to
1-2 years
Significantly reduces in acute phase PSGN
Normalizes after 6-8 weeks
C3 Complement
MRI of PSGN demonstrates
Posterior reversible encephalopathy syndrome (PRES)
If with acute renal insuffiency
nephrotic syndrome
negative strep infection
hematuria + proteinuria
diminished renal function
persistent hypocomplementenemia >2 months
perform
Renal biopsy
Also differentiates APSGN from HSP
PSGN Complications
Hypertensive encephalopathy (Posterior reversible encephalopathy syndrome)
Heart failure and pulmonary edema
Acute renal failure
PSGN Tx
Penicillin G 10d
Sodium restriction
Furosemide
HTN control (CCB, vasodilator)
PSGN Prognosis
Self limiting
Resolution in >95%?
CRD in <2%
Adolescent Edema and joint pains of 2 weeks On and off fever of 1 month Rashes of 2 weeks Dec urine output
BP= 160/100 Pallor Tachycardic Bilateral bipedal edema Swollen ankles
SLE
Majority are adolescent females (connected with estrogen)
Immune complex mediated
Autoantibodies directed at Nuclear antigens
SLE
Most important cause of morbidity and mortality in SLE
Glomerulonephritis >80%
ACR SLE Clinical Criteria
Acute cutaneous lupus (malar) Chronic cutaneous lupus (discoid) Oral or nasal ulcer Non scarring alopecia Synovitis >/=2 joints Renal Hemolytic anemia Leukopenia or lymphonia Thrombocytopenia
ACR SLE Immunologic Criteria
ANA Anti dsDNA Anti-smith APAS Low complement Direct coomb
SLE Diagnosis should fulfill
4/11 criteria +
one biopsy showing lupus
If renal biopsy + and only 2, still lupus
Classification of Lupus Nephritis
I - minimal mesangial (no renal findings)
II - mesangial proliferative (mild, minimal urinary sediment, active serology)
III - focal proliferative (proteinuria 25%; HTN)
a) active
a/c) active/chronic
c) chronic
IV - diffuse proliferative (most severe renal, nephrotic; dec GFR)
V - membranous LN GN (significant proteinuria; less active serology)
VI - advanced sclerosing LN (>90% glomerulosclerosis)
SLE Tx
Prednisone 1-2mkd 4-6weeks over 4-6 months
Monitor via C3, urinalysis, proteinuria
Others Cyclophosphamide 6 months Methylprednisone 6 months Mycophenolate mofetil Rituximab
Hydroxychloroquine (Plaquenil) for extrarenal manifestatikns
ACEI/ARBs
SLE prognosis
10 year survival in 80%
Risk of infection, osteoporosis, poor growth from immunosupression
Most common cause of UTI in children for both sexes
E coli
Presence of bacterial pilli or fimbriae on bacterial surface
Cytitis with gross hematuria is usually caused by
Adenovirus
In children, incidence in <1 is higher in
Males bec of prepuce and hygiene but by 1-2, F predominance
Positive urine culture without any manifestation
Only alarming in pregnant
On UA, patients have leukocytes
Culture must still be done
Asymptomatic bacteriuria
UTI Confirmatory test
Urine CS > 50,000 single colony in suprapubic tap
Urine CS >10,000 cath sample with symptoms
Urine CS >100,000 single colony in bag
Patients <6 months with febrile UTI order
UTZ within 6 weeks of infection
VCUG if abnormal UTZ
Recurrent infections - CMSA scan
Patients >6 months
UTZ for atypical and recurrent UTI
UTZ dilatation etc - VCUG
Pyelonephritis Tx
Younger children:
Ceftriaxone IV
Cefotaxime IV
Ampicillin IV + Gentamycin IV
Without warning sign:
Cefixime PO
Adolescent >17
Fluoroquinolone
Acute febrile - 7-14 days
Acute Cytitis Tx
TMP-SMZ (E coli) for 3-5 days
Amoxicillin
Initial but high resistance - Nitrofurantoin (Kleb, Enterobacter) 3-5 days
2 episodes of UTI, within 6 months:
Vesico-ureteral reflux
UT obstruction
Neuropathic bladder
Urinary calculi
Congenital and familial
Retrograde flow of urine from bladder to kidney
Reflux nephropathy -> CKD
Vesico-ureteral reflux
Classification:
Primary - congenital incompetence of the valvular mechanism of VUJ
Primary with malformation - ureteral duplication, ureterocoele, ureteral ectopia, paraureteral diverticula
Secondary to inc intravesical pressure - neuropathic bladder, BOO, non-neuropathic bladder
Secondary to inflamm - foreign bacterial cystitis, foreign bodies, vesical calculi, clinical cystitis
Secondary to surgical procedure - surgery
Grading of VUR
Grade I - VUR into a non-dilated ureter
Grade II - VUR in upper collecting without dilation
Grade III - VUR into dilated ureter and/or blunting of calcyeal fornices
Grade IV - VUR into a grossly dilated ureter
Grade V - Massive VUR, significant ureteral dilation and tortuosity
VUR Tx
Grade I and II - observation, modification
Grade III and IV - antimicrobial prophylaxis
Sx
Open ureteral reimplantation
Laparoscopic VUR
8/M
Hematuria on UA
B Flank mass since infancy
UTZ: enlarged kidneys with bilateral MACROCYST
UTI
BP: 160/100
Polycystic Kidney Disease
fatal on neonatal period
Most common hereditary human kidney disorder
Possible CYST formation in liver, pancreas, spleen, brain and cerebral aneurysm
CAUSED BY MUTATIONS ON
PCK
PKD1 Ch16 short arm
PKD2 Ch4 long arm
PCK Tx
Control HTN using ACEI/ARB
4/F
Cough of 5 days
Edema of 2 days
Facial edema, ascites, bipedial edema
UA: 3+ proteinuria
Idiopathic Nephrotic syndrome
Most common
Glomerular disease with isolated proteinuria
Peaks in 2-6 years
Heavy proteinuria >3.5 g/24h Urine protein/creatinine ratio >2 Hypoalbuminemia of =2.5 g/dL Edema Hyperlipidemia >200 mg/dl
Nephrotic syndrome
Most common cause of nephrotic syndrome in children
Minimal change disease
Children <2 years old
Edema
Proteinuria
Resistant to prednisone
Congenital Primary Nephrotic Syndrome
Preceded by minor infection (insect bite, allergic reaction)
Foot process effacement
Increased permeability of glomerular capillary wall
Protein leakge in urine (hypoalbuminemia, proteinuria)
Hyperlipidemia (inc synthesis and, dec catabolism) from albumin production
Minimal change disease
Patients with MCD have increased susceptibility to infection because
urinary losses of IgG and complement factors
impaired opsonization of microorganism
Hemodynamic change in MCD
Hypercoagulability from vascular stasis, hemoconcentration, increased platelet number and aggregability and changes in coagulation factor
Increased Fibrinogen
Antithrombotic factors
Deep vein thrombosis
MCD Tx
Prednisone for 4-6 weeks Sodium restriction <1500 Diuretics Dyslipidemia (HMG CoA reductase) 3rd gen cephalosporin infection Heparin; LMW and warfarin for thromboembolism
10/M
Weakness of both Lower extremities
Polyuria
Weight z score: -1 to -2
Mild signs of dehydration
Tubular disease
volume and electroylte abnormality
If acidotic Renal tubular acidosis
Normal anion gap
Hyperchloremic metabolic acidosis
Renal Tubular Acidosis
RTA Types
Proximal RTA - type II
Classic Distal RTA - type I
Hyperkalemic RTA - type IV
Combined proximal and distal RTA - type III
Impaired bicarbonate reabsorption
Normal anion gap Hyperchloremic Metabolic Acidosis
Urine pH <5.5
Normal to low plasma K
Rickets
Proximal Type II
Defect at proximal tubule
Can acidify urine
Rickets because calcium is reabsorbed at proximal part. Because of defect, low electrolyte and calcium
Failure to secrete acid secretion
Normal anion gap Hyperchloremic Metabolic Acidosis
Urine pH >5.5
Normal to low K
Hypercalciuria
Nephrocalcinosis on UTZ
Classic Distal Type I
Cannot acidify urine
Impaired aldosterone production response
Normal anion gap Hyperchloremic Metabolic Acidosis
Urine pH <5.5
High plasma K
High urine Na
Low urine K
Hyperkalemic Type IV
Anion gap formula
Na - (Cl + HCO3)
Urine anion gap
(Urine Na + Urine K) - Urine Cl
RTA Tx
Bicarbonate replacement
20 - Proximal Type II
2 - Distal Type I
Thiazide for hypercalciuria and nephrocalcinosis to decrease calcium excretion
Failure to thrive
Polyuria
Recurrent episodes of Dehydration
Metabolic alkalosis Hypercalciuria Hypokalemia Normal Magnesium Salt wasting
Barter syndrome
Mutation in transporters in the LOH
Hypokalemic
Metabolic alkalosis
Hypercalciuria
Salt wasting
Bartter syndrome
Type I, II, IV - antenatal
Classic - childhood
Hypocalciuria
Hypomagnesemia
Hypokalemia
Metabolic alkalosis
SPASM and TETANY
Gitelmann Syndrome
Rare autosomal recessive
Bartter Tx
Gitelmann Tx
Barter:
K supplement
Prevent dehy
Gitelmann:
K and Mg supplement
6 year old
Vomiting and diarrhea of 3 days
Decreased activity and appetite
Last UO 8 hours PTA
Acute Kidney Injury
Sudden deterioration of renal function
Inability of kidney to maintain fluid and electrolyte homeostasis
pRIFLE
Acute Kidney Injury
AKI Risk criteria
<0.5 ml/kg/hr for 8 h
25% dec in CO
AKI Injury
<0.5 ml/kg/h for 16 h
Dec 50% CO
AKI Failure
<0.3 ml/kg/h for 24 h
Anuric for 12h
Dec by 75% CO
eCCl <35ml/min/1.73m2
AKI Loss
Persistent failure >4 weeks
AKI End stage
Persistent failure >3 months
Pre Renal AKI
Dehydration Hemorrhage Sepsis Hypoalbuminemia Cardiac failure
Intrinsic Renal
GN Hemolytic Uremic Syndrome Acute tubular necrosis Cortical necrosis Renal vein thrombosis Rhabdomyolysis Acute Interstitial Nephritis Tumor infiltration Tumor lysis syndrome
Post Renal AKI
Posterior urethral valve Ureteropelvic junction obstruction Ureterovesicular junction obstruction Ureterocoele Tumor Urolithiasis Hemorrhagic cystitis Neurogenic bladder
Biomarkers for AKI
Plasma neutrophil gelatinase-associated lipocalin Cystatin C Urinary NGAL IL-18 Kidney injury molecule-1
U Specific gravity >1.020
U osmolality >500
U Na <20
U Fractional excretion of Na (FENa) <1%
Prerenal AKI
Kidney able to compensate. Because dehydrated, osmolality is high and urine sodium low to retain water hence concentrated urine.
U specific gravity <1.010
U osmolality <350
U Na >40
Fractional excretion of Na (FENa) >2%
Intrinsic AKI
No compensation
Hyperkalemia Metabolic Acidosis Hypervolemia Hypertension Anemia
Acute Kidney Injury
AKI Tx
Diuretics - hypervolemia (edema)
Ca Gluconate, NaHCO3, Insulin + D50 - hyperkalemia
NaHCO3 - metabolic acidosis
salt-water restriction, Ca ch blocker - HTN
blood transfusion, iron or EPO - anemia
Indications in AKI for dialysis
Anuria/oliguria
Volume overload with hypertension and/or pulmonary edema refractory to diuretic therapy
Persistent hyperkalemia
Severe metabolic acidosis unresponsive to medication
Uremia (encephalopathy, pericarditis, neuropathy)
BUN > 100-160 mg/dl
Ca:P imbalance with hypocalcemic tetany
16/F
Pallor
Edema
Periorbital edema
BP: 120/90
Stunted
growth retarded
Chronic Kidney Disease
Clinical manifestations: Edema Hematuria Headache Anorexia Hypertension Proteinuria Fatigue Growth failure/Anorexia
Elevated BUN/Crea Hyperkalemia Hyperphosphatemia Hyponatremia Acidosis Hypocalcemia Elevated uric acid
CKD Diagnosis
Kidney damage >/= 3 months (structural or functional abnormalities of kidney with or without decreased GFR)
GFR <60 mL for >/= 3 months
(with or without other signs of kidney damage)
CKD stages
Stage 1 - GFR >90 Stage 2 - GFR 60-89, mild dec in GFR Stage 3 - GFR 30-59, mod dec in GFR Stage 4 - GFR 15-29, severe dec in GFR Stage 5 - GFR <15, kidney failure
CKD tx
Acidosis - NaHCO3
Growth - recombinant human growth hormone
Bone disease - CaCO3, Phosphate binder, Vit D analog
Anemia - Erythropoietin Stimulating Agents
HTN - diuretics, ACEI/Arb
Advise the patient for renal transplantation
On the average, symptoms of uncomplicated PSGN resolve within
6-8 weeks
Urinary protein excretion and HTN - 4-6 weeks
Microscopic hematuria - persist 1-2 years
disease with decreased serum complement c3
SLE Subacute bacterial endocarditis Shunt nephritis Essential mixed cryoglobulinemia Visceral abscess PSGN Membranoproliferative GN Type I