The Kidney - LSH Student Resources

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Transcript The Kidney - LSH Student Resources

The Kidney
Definitions
Azotemia – Increased BUN and creatinine, usually
related to decreased GFR
Pre-renal azotemia – hypoperfusion of the kidneys
Post-renal azotemia – obstrution to urine flow
Uremia – azotemia plus other metabolic and
endocrine alterations resulting from renal
damage
Definitions
Nephritic syndrome – glomerular disease, hematuria, RBC
casts, mild to moderate proteinuria, hypertension,
oliguria, edema
Rapidly progressive glomerulonephritis- nephritic syndrome
with rapid decline (hours to days) in GFR
Nephrotic syndrome – glomerular disease, proteniuria >3.5
gm per day, hypoalbuminenia, severe edema,
hyperlipidemia, lipiduria, inreased risk of infection,
inreased risk of thrombosis, renal vein thrombosis
Definitions
Acute renal failure – rapid and frequently
reversible onset, oliguria or anuria and
recent onset of azotemia
Chronic renal failure – Prolonged symptoms
and signs of uremia
Definitions
Diminished renal reserve
GFR 50% of normal,
Asymptomatic
Renal insufficiency
GFR 20%-50% of normal, azotemia, anemia,
hypertension, decreased concentrating ability
leading to polyuria and nocturia
Chronic renal failure
GFR < 20% of normal, volume and solute
composition cannot be regulated, edema,
metabolic acidosis, hyperkalemia, overt uremia
End-stage renal disease
GFR < 5% of normal, terminal stage of uremia
Chronic Renal Failure
Fluid and Electrolyte
Dehydration
Edema
Hyperkalemia
Metabolic acidosis
Calcium, Phosphate,
Bone
Hyperphosphatemia
Hypocalcemia
Secondary hyperparathyroidism
Renal osteodystrophy
Hematologic
Anemia
Bleeding diasthesis
Cardiopulmonary
Hypertension
CHF
Cardiomyopathy
Pulmonary edema
Uremia pericarditis
Chronic Renal Failure
Gastrointestinal
Nausea and Vomiting
Bleeding
Esophagitis, gastritis, colitis
Neuromuscular
Myopathy
Peripheral neuropathy
Encephalopathy
Dermatologic
Sallow color
Pruritus
Dermatitis
Glomerular Diseases
Acute Proliferative Glomerulonephritis- ( poststreptococcal)
1-4 weeks after a strep infection ( pharynx or skin)
Most frequently -6-10 years of age
Malaise, fever, nausea, oligouria, hematuria, RBC casts, mild proteinuria,
periorbital edema, mild to moderate hypertension
Immune complex mediated disease
Enlarged, hypercellular glomeruli
Granular deposits
Serum complement is decrease. ASO and other anti-strep antibodies are
increased
EM – subepithelial humps
Adults tend to present with sudden hypertension and/or edema and elevated
BUN
Glomerular Diseases
Rapidly progressive ( crescentic ) GNRapid and progressive loss of renal function
Formation of crescents- proliferation of parietal cells,
infiltration of WBCs into the urinary space, compress the
glomerular tuft, obliterate Bowman capsule
Rupture of the GBM
Type I anti-GBM, e.g. Goodpasture syndrome
Type II Immune complex, e.g. Post-infectious GN
Type III pauci-immune ANCA, e.g. Wegener
granulomatosis
Causes of Nephrotic Syndrome
Primary Glomerular
Membranous
Minimal-change
Focal segmental
glomerulosclerosis
Membrano-proliferative
Other – e.g. IgA nephropathy
Systemic
DM
Amyloidosis
SLE
Drugs- NSAIDs, penicillamine,
heroin
Infections – malaria, syphilis,
HBV, HCV,HIV
Malignant disease
Misc – e.g. hereditary nephritis
Minimal Change Disease
Most frequent cause of nephrotic syndrome
in children
Visceral epithelial cells- uniform and diffuse
effaement of foot processes
Immunoflorescence is negative
Membranous Nephropathy
Common cause of nephrotic in adults
Diffuse, uniform thickening of the glomerular
capillary wall
Granular immunoflorescence
Subepithelial deposits
Focal Segmental
Glomerulosclerosis
Most common form of nephrotic syndrome in
adults
Collapsing glomerulopathy – HIV associated
Loss of foot processes
Epithelial damage
Membranoproliferative GN
Alterations in the GBM
Proliferation of glomerular cells
Leukocyte infiltration
Also called mesangiocapillary GN
Type I Immune complexes and activation of both classical
and alternative complement pathways, subendothelial
deposits
Type II dense-deposit disease activation of the alternative
complement pathway
IgA Nepropathy (Berger Disease)
IgA deposits in the mesangial regions
Frequent cause of recurrent gross or microscopic
hematuria
Probably the most common cause of GN
worldwide
Henoch-Schonlein purpura
Secondary- liver disease and gluten enteropathy
Alport Syndrome
Hereditary nephritis
Hematuria with progression to chronic renal
failure
Nerve deafness
Various eye disorders ( e.g. lens dislocation)
Abnormalities of alpha chains in type IV
collagen
Benign Familial Hematuria
Hereditary nephritis
Asymptomatic hematuria
Diffuse thinning of the GBM
Renal function is normal
Prognosis is excellent
Lupus Nephritis
Type I – No renal involvement ( mild mesangial)
Type II – Mesangial form – granular mesangial
deposits of immunoglobulin and complement
Type III – Focal-proliferative Type IV – Diffuse proliferative ( most severe) crescentic
Type V – Membranous – thickening of GBM
Diabetic Glomerular Nephropathy
Widespread thickening of the GBM
Diffuse increase in mesangial matrixexpansion of the mesangium correlates
with measures of deteriorating renal
function
Nodular glomerulosclerosis – KimmelsteilWilson disease
Tubular and Interstitial Diseases
AKI ( ATN)
Acute diminution of renal failure,
and often morphologic
evidence of tubular injury
Most common cause of Acute
renal failure
Tubular injury and persistent and
severe disturbances in blood
flow
Causes – Ischemia, direct toxic
injury, acute tubulointerstitial
nephritis, urinary obstruction
Initiation, maintenance, recovery
phases
Tubulointerstitial nephritis
Causes- infections, toxins,
metabolic diseases, physical
factors, neoplasms,
Immunologic
reactions,vascular diseases,
miscellaneous
Pyelonephritis and UTI
Lower track – frequency, urgency, pyuria, dysuria, hematuria,
Upper track ( pyelo) – fever leukocytosis, CVA tenderness, WBC casts
in urine
patchy interstitial suppurative inflammation, intratubular aggregates
ofn neutrophils, tubular necrosis, Papillary necrosis, pyonephrosis,
perinephric abscess, pyelonephritic scar-inflammation, fibrosis,
deformation of underlying calyx and pelvis
E. Coli most common
Ascending infection
VUR, obstruction, instrumentation, pregnancy, preexisting renal lesions,
DM, immunosuppression
Vascular Diseases
Benign nephrosclerosis- hyaline arteriosclerosis
Malignant nephrosclerosis – fibrinoid necrosis and
onion-skinning
Renal artery stenosis – most common cause is
atherosclerosis, fibromuscular dysplasia
Renal infarction – white – end-organ
Thrombotic Microangiopathies
Microangiopathic hemolytic anemia
Thrombocytopenia
Renal failure ( in many cases)
Thrombotic lesions in capillaries and arterioles
Endothelial injury
Platelet aggregation
Typical ( epidemic, classic, diarrhea-positive) HUS- Shiga-like toxins, E.
coli 0157:H7
Atypical ( non-epidemic, diarrhea-negative) HUS- genetic mutations in
complement-regulatory factors, antiphospholipid syndrome,
postpartum, vascular diseases, drugs, irradiation
Thrombotic Thrombocytopenia Purpura – ADAMTS13, CNS
involvement dominant
Cystic Diseases
Adult polycystic kidney disease – AD, CRF
later in life, berry aneurysms, hepatic
cysts,MVP and other valvular lesions
Childhood polycytic kidney disease- AR,
Death in infancy or childhood, hepatic
fibrosis
Urinary Tract Obstruction
Common causes:
Congenital anomalies
Urinary calculi
BPH
Tumors
Inflammation
Sloughed papillae or blood clots
Pregnancy
Uterine prolapse and cystocele
Functional disorders – neurogenic bladder
Hydronephrosis – Dilation of the renal pelvis and calyces associated with
progressive atrophy of the kidney due to obstruction to the outflow of urine
Obstruction also triggers an interstitial inflammatory reaction, leading eventually
to interstitial fibrosis
Urolithiasis
Calcium stones- oxalate and/or phosphate
Triple stones – magnesium ammonium
phosphate, infections, staghorn calculi
Uric acid stones
Cystine
Tumors
Renal cell carcinoma – adenocarcinoma. Smoking, obesity,
unopposed estrogen,
Asbestos, petroleum products, heavy metals
CRF, acquired cystic disease, tuberous
sclerosis
von Hippel-Lindau
Clear cell- 70-80%
CVA pain, palpable mass, hematuria
Paraneoplastic syndromes, widespread metastases
before local signs and symptoms