Renal Diseases Flashcards
Azotemia
Elevation of the blood urea nitrogen (BUN) and creatinine levels, due to decreased filtration of blood through the glomeruli (decreased glomerular filtration rate).
Uremia
Association of azotemia with clinical signs and symptoms, including gastroenteritis, peripheral neuropathy, pericarditis, dermatitis, hyperkalemia, and metabolic acidosis. advanced form of liver disease
Azotemia is due to ________
decrease glomerular filtrate
you get increased levels of ____ and ____ in azotemia
nitrogen and creatinine
Major Clinical Renal Syndromes
Acute nephritic syndrome
Nephrotic syndrome
Acute renal failure (rapidly)
Acute nephritic syndrome
Results from glomerular injury and is characterized by acute onset of hematuria (blood in urine), mild to moderate proteinuria, azotemia, and hypertension.
Nephrotic syndrome
Glomerular syndrome characterized by heavy
proteinuria (> 3.5 grams per day), hypoalbuminemia, severe edema, hyperlipidemia, and lipiduria.
nephritic associated simply with ____ in urine
blood
nephrotic associated simply with ____ in urine
protein
Acute renal failure
Acute onset of azotemia with oliguria (or anuria). (inability to produce urine)
CONGENITAL CYSTIC KIDNEY DISEASE (2)
Autosomal dominant (adult) polycystic kidney disease Autosomal recessive (childhood) polycystic kidney disease
auto dominant associated with ____ (age group)
adult
auto recessive associated with ____ (age group)
children
Autosomal dominant (adult) polycystic kidney disease clinical presentation
characterized by MULTIPLE EXPANDING CYSTS in BOTH kidneys. Gradual onset of renal failure in adult, urinary tract hemorrhage (hematuria), pain, hypertension, urinary tract infection.
Autosomal dominant (adult) polycystic kidney disease etiology
defective gene is PKD1 (in 90% of families) located on chromosome 16. The gene encodes for polycystin-1
Autosomal dominant (adult) polycystic kidney disease Extrarenal pathology
1/3 of patients have CYSTS IN LIVER; aneurysms
may develop in the circle of Willis (intracranial)
Autosomal dominant (adult) polycystic kidney disease Pathology
very large (up to 4 kg) kidneys with numerous cysts that
arise in every part of the tubular system
BIG KIDNEYS
Autosomal recessive (childhood) polycystic kidney disease clinical presentation
renal failure develops from infancy to several years of age – rare; seen in 1 in 20,000 live births.
Autosomal recessive (childhood) polycystic kidney disease extrarenal pathology
almost all have liver cysts and progressive liver fibrosis
Autosomal recessive (childhood) polycystic kidney disease pathology
numerous small uniform-size cysts from collecting tubules in cortex and medulla
Autosomal recessive (childhood) polycystic kidney disease etiology
Due to mutations in the PKHD1 gene
Mechanisms of glomerular injury
- Immune complex deposits in glomerular basement membrane (GBM)
or mesangium. - Epithelial and endothelial cell injury.
Pathologic evaluation of kidney biopsies
- Light microscopy
- Immunofluorescence
- Electron microscopy
Nephrotic syndrome 4 manifestations
- Minimal change disease
- Focal and segmental glomerulosclerosis
- Membranous nephropathy (glomerulonephritis)
- Glomerular disease in diabetes mellitus
Minimal change disease- nephrotic
- most common nephrotic in KIDS
- normal histology of glomeruli
- good response to treatment (in kids)
Focal and segmental glomerulosclerosis- nephrotic
- one of the most common causes of nephrotic syndrome in ADULTS
- may be primary (idiopathic) or secondary to other glomerular diseases, loss or scarring of other glomeruli, or genetic.
- pathology - partial (segmental) sclerosis of some (focal) glomeruli characterized by increased mesangial matrix collagen with obliteration of capillary loops. The idiopathic form has NO immune complexes.
- poor response to corticosteroid treatment – renal failure in 50% after 10 yrs.