NEPHRO Chap 508-536 Flashcards by Karen Morales

At least 5 RBC in urine

Hematuria

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MC chronic glomerular disease in children

IgA Nephropathy

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Focal and segmental mesangial proliferation and ibcreased mesangial matrix

IgA Nephropathy

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Renal histo: epithelial crescent formation and sclerosis

IgA Nephropathy

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Gross hematuria that occurs 1-2 days after an upper respiratory or GI infection
(+) loin pain
Normal C3

IgA Nephropathy

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Nephritis associated with gene mutations for Type IV collagen

Alport Syndrome (Hereditary Nephritis)

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Renal histo:
- mesangial proliferation and capillary wall thickening leading to PROGRESSIVE GLOMERULAR SCLEROSIS
- diffuse thickening, splittinh and layering of glomerular and tubular basement membranes
(+) FOAM CELLS (lipid containing tubular or interstitial cells)

Alport Syndrome (Hereditary Nephritis)

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Asymptomatic microscopic hematuria, intermittent
1-2 days after URTI
Bilateral SENSORINEURAL HEARING LOSS (NEVER CONGENITAL)
ANTERIOR LENTICONUS
(+) family history of renal disease

Alport Syndrome (Hereditary Nephritis)

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Sudden onset of GROSS hematuria, edema, hupertension and renal insufficiency
(+) history of yhroat or skin infection

Renal histo: lumpy bumpy appearance of glomerulus

Low C3

Post streptococcal Glomerulonephritis

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Weeks to develop GN post strep pharyngitis

1-2 weeks after

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Weeks to develop GN post strep pyoderma

3-6 weeks

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Urinary protein excretion and hypertension normalizes by… in GN

4-6wks

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Serum C3 level normalizes by… in GN

6-8 weeks

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Microscopic hematuria persists for… in GN

1-2 years after

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Renal histo: diffuse thickening of basement membrane WITHOUT cell proliferative changes

Electron Microscopy (EM): granular deposits of IgG and C3

NEPHROTIC SYNDROME with RENAL VEIN THROMBOSIS

Membranous Nephropathy

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GN associated with Hepatotis B and Syphilis

Membranoproliferative Glomerulonephritis (MPGN)

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MC Membranoproliferative Glomerulonephritis

Renal histo: accentuated lobular pattern of glomeruli

Type I MPGN

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Type of MPGN with prominent C3 immunofluorescence

EM: lamina densa is very dense WITHOUT evident immune-complex deposit

Markedly depressed C3

Type II MPGN

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MPGN associated with partial lipodystrophy (diffuse loss of adipose tissue and decreased complement

Type II MPGN

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Gold standard for establishing SLE nephritis

Kidney biopsy

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Classification of nephritis?

No histologic abnormalitis but with present mesangial immune deposits

WHO Class I nephritis

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Classification of nephritis?

Mesangial hypercellularity with deposits

WHO Class II nephritis

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Classification of nephritis?

Mesangial and endocapillary lesions with <50% of glomeruli involvement

WHO Class III nephritis

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Classification of nephritis?

Mesangial and endocapillary lesions with >50% of glomeruli involvement

WHO Class IV nephritis

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Monitoring for HSP Nephritis

Urinalysis weekly during active disease then | Monthly up to 6 months

Hallmark of Rapidly Progressive GN

Crescents in glomeruli | *proliferation of epithelial cells in Bowman's space

Pulmonary hemorrhage and Glomerulonephritis

Goodpasture disease

Pulmonary hemorrhage and Glomerulonephritis

Goodpasture disease

Kidney biopsy: cresenteric GN Immunofluorescence: continuous linear deposition of IgG along BM Serum ANTI-GBM antibody is present Normal C3 ANCA elevated

Goodpasture Disease

Triad of Microangiopathic hemolytic anemia, thrombocytopenia and renal insufficiency

Hemolytic Uremic Syndrome

Most common form of HUS

Diarrhea associated HUS (E. coli)

Approved treatment for atypical HUS

Eculizumab

Unilateral bleeding of the left ureter due to compression of the left renal vein (mesoaortic compression) Persistent hematuria, left lower abdominal pain, orthostatic hypotension

Nutcracker syndrome

Thrombus formstion due to endothelial injury secondary to hypoxia, endotoxin or contrast media SUDDEN ONSET of GROSS HEMATURIA & UNILATERAL or BILATERAL FLANK MASSES UTZ: Marked renal enlargement Radionuclide study: no renal function of affected kidney

Renal vein thrombosis

Thrombus formation due to endothelial injury secondary to hypoxia, endotoxin or contrast media SUDDEN ONSET of GROSS HEMATURIA & UNILATERAL or BILATERAL FLANK MASSES UTZ: Marked renal enlargement Radionuclide study: no renal function of affected kidney

Renal vein thrombosis

Treatment of Renal Vein thrombosis

Heparin

Severe hypertension secondary to RVT refractory to medications Tx?

Nephrectomy

Autosomal dominant | Recurrent gross hematuria, persistent microscopic hematuria, dysuria in the ABSENCE of STONE FORMATION

Idiopathic hypercalciuria *Dx: 24h urine calcium >4mg/kg Spot urine Ca:crea >2 *Tx: Hydrochlorothiazide 1-2mg/kg/24h single morning dose

Main site of electrolyte reabsorption

Proximal tubule

Promotes calcium reabsorption

``` Parathyroid hormone Calcitonin Vitamin D Thiazide diuretics Volume depletion ```

Promotes calcium excretion

Volume expansion Increased sodium intake Diuretics

Sites of bicarbonate reabsorption

Proximal tubule | Collecting tubule

``` Proximal Renal Tubular acidosis (pRTA) Ocular abnormalities Short stature Enamel defects Intellectual impairment Basal ganglia calcification ```

Isolated autosomal recessive pRTA

``` Proximal RTA Low molecular weight proteinuria Glycosuria Phosphaturia Aminoaciduria ```

Fanconi syndrome

Defect in metabolism of cysteine leading to accumulation of cystine crystals in major organs

Cystinosis

Most sever form of cystinosis

Infantile or Nephropathic cystinosis * 1st 2 years of life * growth failure and severe tubular dysfunction

Treatment of cystinosis

Cysteamine | - binds to cystine and converts it to cysteine

NAGMA Growth failure Phosphate and bicarbonate wasting Urine is acidic (pH<5.5)

Proximal RTA (Type II)

``` NAGMA Growth failure Severe metabolic acidosis NEPHROCALINOSIS HYPERCALCIURIA Hypokalemia Urine pH>6 ``` May be associated with sensorineural deafness

Distal RTA (Type I)

Cystic dilation of terminal portions of collecting ducts | Medullary calcinosis on UTZ

Medullary sponge kidney

Hyperkalemia Hypoaldosteronism (impaired aldosterone production) or Pseudohypoaldosteronism (impaired renal responsiveness to aldosterone) Hyperkalemic NAGMA

Hyperkalemic RTA (Type IV)

Formula for anion gap

Na - (Cl + HCO3)

Normal anion gap

12-20

Formula for urine anion gap

(Urine Na + Urine K) - urine Cl

Mainstay of therapy for RTA

Bicarbonate replacement

Inability to concentrate urine

Nephrogenic DI

Polyuria, hypernatremia, diluted urine Serum Osm >/=290 Urine Osm <290

Nephrogenic DI

Hypokalemic Metabolic Alkalosis HYPERCALCIURIA Salt wasting Recurrent episidoes of dehydration *maternal history of polyhydramnios8 Urinary calcium, sodium and potassium are ELEVATED Serum renin, aldosterone and prostaglandin E are ELEVATED

Bartter Syndrome

Hypokalemic Metabolic Alkalosis HYPOcalciuria HYPOMAGNESEMIA Late childhood Recurrent muscle cramps and spasms *DO NOT have history of recurrent dehydration Urinary Calcium is LOW Urinary Magnesium is ELEVATED

Gitelman Syndrome

Associated with Rickets

Proximal RTA

Tubulointerstitial inflammation & damage with relative sparing of glomeruli

Tubulointerstitial nephritis (TIN)

``` Fever, rash and arthralgia (1-2 weeks after antibiotics) Rising serum creatinine Flank pain Nonoliguric Normotensive ``` UA: white blood cell casts Lymphocytic infiltration of tubulointerstitium, tubular efema and tubular damage

Acute TIN *rbc casts (sign of glomerular disease) are absent

Type of TIN that presents with nephrotic syndrome

Acute TIN secondary to NSAIDs

T/F: Corticosteroid administration within 2 weeks of the discontinuation of the offending agent can hasten recovery and improve long-term prognosis in drug-induced TIN

True

Most important factor predicting progression to ESRD in Chronic TIN

Severity of interstial disease

Nephrotoxic? ACE Inhibitors

Yes. Causes Nephrotic syndrome Acute renal failure

Nephrotoxic? ACE Inhibitors

Yes. Causes Nephrotic syndrome Acute renal failure

Nephrotoxic? Amphotericin

Yes. Causes Nephrogenic DI Acute renal failure Renal tubular acidosis

Newborn Massive polyuria, volume depletion, hypernatremia, hyperthermia Irritabile Constipation Poor weight gain despite adequate caloric supplementation Behavioral problems

Congenital Nephrogenic DI

Rare cause of acute renal failure secondary to extensive ischemic damage to renal cortex Commom in neonates (hypoxic or ischemic insult) and adolescents (+) Hypertension Hematuria, proteinuria on UA Anemia and thrombocytopenia

Cortical necrosis