Renal and Metabolic Disease

congestive heart failure : organs cannot get perfused, not enough pressure to the kidney

1. glomerular
2. tubular
3. interstitial
4. vascular

results from toxic or infectious substances

results from toxic or infectious substances

caused by a reduction in renal perfusion that induces morphologic and functional changes in kidney

losing BP: afferent does not have enough force to push and filter the blood through the glomerulus; BP too strong then too much is forced through

immunologic, metabolic, and hereditary

systemic diseases from other organs that affect kidney

specifically affect kidney, only organ involved

glomerulonephritis

cells in PCT die, leading to polyuria
recall cells in PCT absorb glucose, AA, water

1. cellular proliferation
2. leukocytic infiltration
3. glomerular basement thickening
4. hyalinization with sclerosis

increased numbers of endothelial cells (&others) in glomerular tuft causes a problem with flow of filtrate at bowman's capsule

drawn by local chemotactic response (inflammation and swelling, infection) which damages glomerulus

recall: filtration needs to be thin to allow proper things to pass through
*any process that results in enlargement of basement membrane
usually in response to antibodies (ex. Anti-GBM)

glomerular basement thickening

autoimmune disease where immune system makes anti-GBM, leading to blood in urine AND sputum (lungs)

accumulation of homogenous eosinophilic extracellular material
(form of scarring, like leaving wet dog pebble food out too long and it forms together)
scarred tissue loses function

hematuria
proteinuria
oliguria
azotemia
edema
HTN

disease causes glomerulus to be so porous that even large molecules (like RBC and protein) to be pushed through

increased nitrogen (urea, creatinine, uric acid) in blood

if glomerulus is porous, losing proteins (albumin); the oncotic pressure is not enough and the fluid stays in the interstitial space

edema (more fluid in body), blood vessels cant change diameter as easily

heavy proteinuria >3.5 g / day

hypoproteinemia (&hypoalbuminemia) due to loss of protein in urine

kidney diseases that affect tubules and interstitial, like interstitial nephritis because only the GLOMERULUS is affected

because the podocytes retract, allowing larger molecules to pass through

hyperlipidemia and lipiduria, oval fat bodies present, cholesterol, triglycerides

the liver produces triglycerides and cholesterol due to protein loss

1. hematuria
2. oliguria
3. azotemia
4. HTN

damage is within glomeruli (due to inflammation damaging the glomeruli walls), allows RBC and WBC infiltration into urine. Leads to decreased GFR (seen as oliguria and azotemia), HTN result of fluid retention and increased renin released from ischemic kidney

Strep A beta hemolytic affect glomerular membrane; produces toxin that attacks glomerular

sclerosis hyalinization due to thickness, crescent of proliferating cells around glomerulus; leads to obstruction of pathway and decreased GFR

disease that affects podocytes, most common in adults

disease that affects podocytes, most common in children

the damage is focal, damage is only to specific part of glomerulus

When space in bowman's capsule is lost, causing pathway to PCT to close, filtrate cannot go through

Berger disease

deposits of IgA (?) on the BM side of podocytes, affecting function of the glomerulus

end stage renal failure

systemic lupus erythematosus (SLE), diabetes mellitus, amyloidosis

autoimmune disorder with immune complex deposits, kidney commonly goes into failure as a result

carb metabolism disorder due to lack of insulin or cellular resistance to insulin

group of diseases involving many organs; characterized by deposits of amyloid (junk), a pathologic protein substance

1. acute tubular necrosis (ATN)
2. tubular dysfunction (4 kinds)

ischemic ATN and Toxic ATN

sepsis, shock, trauma

allergies, causing dilation in all blood vessels at the same time so the kidney cant get adequately perfused

from exogenous or endogenous nephrotoxins?

chemotherapy, antibiotic therapy

1. Fanconi syndrome
2. renal glucosuria
3. renal phosphaturia
4. renal tubular acidosis

PCT cells cannot absorb (leading to increase in glucose, aa, protein, polyuria)

mutation that reduces the 'workers' that process glucose, so glucose ends up in the urine although everything else is okay (blood glucose is normal)

body doesn’t absorb calcium phosphate, phosphate being lost in urine

hyperparathyroidism; parathyroid hormone (PTH) works with calcitonin to put calcium and phosphate to bones. But if PTH is elevated, DCT SECRETES (instead of absorbs) phosphates

recall: job of kidney is to maintain pH
pH cannot go below 5.3, blood is acidic and urine is more basic. Kidney is unable to secrete H+

UTI, acute pyelonephritis, chronic pyelonephritis, acute interstitial nephritis (AIN), yeast infections

upper UTI'; usually seen as WBC casts in urine

AIN, usually due to allergic reaction of interstitial cells.
Diagnostic: presence of eosinophils

SUDDEN decrease in GFR, azotemia, and oliguria;
functional abnormality, but no cellular changes
classified as prerenal, renal, and postrenal

Both still increase but at different rates

due to hypertrophy of remaining healthy nephrons, not clinically recognized until 80-85% function is lost
(nephrons will compensate until its too late)

azotemia, acid-base imbalance, abnormal calcium and phosphate metabolism

diabetes, lupus

aggregates of mineral salts in a matrix of proteins and lipids

calcium

renal calyces, renal pelvis, ureters, or bladder

1. supersaturation of chemical salts in urine
2. optimal urinary pH
3. urinary stasis
4. treatment depends on type and size of stones

genetic

interruption of urine -> some solutes come out of solution and induces kidney stones

history of renal calculi, metabolic disturbances, dehydration, sedentary life style, and immobility

cannot process certain things so it becomes supersaturated (and become larger and larger)

problem in TRANSPORTING cystine, cystine stuck in lysosomes, add up and kills PCT cells (leading to Fanconi syndrome)

branched-chain keto acid dehydrogenase mutated, byproducts lead to increase in valine, isoleucine, and leucine (aa); altering pH, affecting CNS

enzyme cant convert to tyrosine, increasing acidity in blood

No enzyme to convert homogentisic acid to CO2 and H2O, leading to an increase in homogentisic acid that gets deposited in tissue and joints
can develop arthritis at a young age

turns black when left exposed to air

hereditary defects of heme synthesis pathway, can possibly lead to lead poisoning.
If not converted, leads to anemia