Disease Correlation

most common etiology (cause) of glomerular disease

immunologic (most common)

metabolic causes

hereditary disorders

what changes occur in the glomerular tissue as a result of glomerular disease

1. cellular proliferation

2. leukocyte infiltration (WBCs go to inflammation)

3. glomerular basement membrane thickening (b/c it’s repairing over and over)

4. hyalinization with sclerosis (tissue is being replaced by scar tissue which hardens)

how does the disease process of glomerular disease occur

antibody-antigen complexs are formed and get stuck and clog the glomerulus so it gets inflammed anf filtration can’t occur

when glomerulus filter is compromised waste begins to build up and end up in the bloodstream

what specific renal disease is most likely to progress to renal failure and require either dialysis or a transplant

acute glomerulaonephritis

common clinical features that all three of the glomerular diseases discussed in class share

hemeturia, proteinuria, oliguria, azotemia, edema, and hypertension

physical/chemical/microscopic findings of acute glomerulonephritis that make it unique

protein: mild (<1 g/day)

increased casts

physical/chemical/microscopic findings of acute glomerulonephritis

protein: mild (<1 g/day)

blood: positive (variable)

increased RBCs, WBCs, renal tubular epi cells

increased casts (RBC/Hgb/granular)

physical/chemical/microscopic findings of chronic glomerulonephritis

protein: heavy (>2.5 g/day)

blood: positive (usually small)

SG: low and fixed (isothenuria)

increased RBCs, WBCs, rnal tubular epi cells

casts (all types but esp grabular/waxy/broad)

physical/chemical/microscopic findings of chronic glomerulonephritis that make it unique

protein: heavy (>2.5 g/day)

SG: low and fixed (isothenuria)

casts (all types but esp. granular/waxy/broad)

physical/chemical/microscopic findings of nephrotic syndrome

protein: severe (>3.5 g/day)

blood: positive (usually small)

oval fat bodies and free fat globules present

increased casts (esp. fatty/waxy/renal cell)

increased RBCs and renal epi cells

physical/chemical/microscopic findings of nephrotic syndrome that make it unique

protein: severe (>3 g/day)

oval fat bodies and free fat globules present

increased casts (esp. fatty/waxy/renal cell)

what glomerular disease is associated with increased lipids present in the urine

nephrotic syndrome

difference between acute and chronic glomerularnephritis

acute: sudden and swelling and blockage inhibits filtration

chronic: occurs over time, glomerular disease has progressed to point of sclerosis (hardening of tissue) and hyalinization (scarring)

difference between ischemic and toxic acute tubular necrosis in terms of the cause of each

ischemic: due to hypovolemic event (decreased BP) where the kidneys have decreaed perfusion (blood flow)

toxic: due to exposure to a toxin (ex: meds/drugs, poison, or heavy metals)

difference between ischemic and toxic acute tubular necrosis in terms of what part of the tubules is affected

ischemic: proximal convoluted, loop of henle, the distal convoluted, and the collecting duct (more likely to affect the basement membrane, and more spread out)

toxic: proximal convoluted, loop of henle, distal convoluted, and collecting duct (more concentrated in the PCT)

acute tubular necrosis clinical features

oliguria, azotemia, uremia, acid-base imbalance, electrolyte imbalace

for acute tubular necorisis, what treatment is there

remove the causitive agent, once ID and removed normally symptoms go away

what is tubular dysfunction

dysfunction of the tubules system either in a small and isolated area or a large and diffuse area that causes a variety of effects (ex: cystinuria, fanconi’s, renal phospaturia)

why is the GFR normal for tubular dysfunction

the filtration system is working, it’s the tubules that aren’t absorbing the filtered substances

examples of tubular dysfunction disorders

cystinuria (PCT can’t absrob cystine)

fanconi’s (PCT doesn’t absorb at all)

renal phosphaturia (PCT doesn’t absorb phosphate)

renal tubular acidosis (tubules can’t secrete enough hydrogen so acid base balance is off)

what region of the urinary tract is affected by urethritis

urethra

what region of the urinary tract is affected by cystitis

bladder

what region of the urinary tract is affected by pyelitis

pelvis

what region of the urinary tract is affected by pyelonephritis

spaces inbetween where filtration occurs (interstition of the kidneys)

why do UTIs affect females more frequenty than males

women due to having a shorter urethra and its close proximity to the anal region, greater hormone fluctuations, and no prostate (prostatic fluids has natural antibacterial effects)

physical/chemical and microscopic findings for urethritis/cystitis

protein: small (<0.5 g/day)

LE: positive

nitrate: usually positive

blood: positive

increased WBCs and RBCs

bacteria

transitional epi cells

physical/chemical and microscopic findings for urethritis/cystitis that make it unique

protein: small (<0.5 g/day)

transitional epi cells

no casts (b/c kidney isn’t involved)

physical/chemical and microscopic findings for pyelonephritis/pyelitis (acute)

protein: mild (<1 g/day)

blood: positive

LE: positive

nitrate: usually positive

SG: normal to low

increased WBCs, bacteria, RBCs, and renal epi cells

increased casts (granular, waxy, broad, WBC, and renal cell)

physical/chemical and microscopic findings for pyelonephritis/pyelitis (acute) that make it unique

protein: mild (<1 g/day)

SG: normal to low

increased renal epi cells

physical/chemical and microscopic findings for pyelonephritis (chronic)

protein: moderate (<2.5 g/day)

LE: may be positive

SG: low (may have isothenuria)

increased WBCs and macrophages

increased worsening casts (granular, waxy, broad, few WBC, and renal cell

physical/chemical and microscopic findings for pyelonephritis (chornic) that make it unique

protein: moderate (<2.5 g/day)

LE: may be positive

SG: low (may have isothenuria)

increased macrophages

increased worsening casts (few WBC ones)

S/S of urethritis/cystitis

pain or burning on urination (dysuria) and occasional lower abdomen pain

S/S of pyelitis/pyelonephritis

flank pain (in back and sides), painful urination (dysuria), nocturia, urgency, fever, nausia, headache, malaise, and polyuria

etiology of chronic pyelonephritis

birth defects

an acute infection that was never treated properly

common causes of interstitial nephritis

exposure to drugs, toxins, and heavy metals (when removed issue fixes)

what three ways can interstitial nephritis affect the interstitial tissues

immediate allergic response

rapid tubules destruction

slowly and progressing failure of the tubules

most common species of yeast associated with yeast infections

Candida species

specific conditions in which a yeast infection is more likely to occur

normal flora being disrupted by a pH change or steroid use (immunocompromised) or antibiotics

introduced via urinary catherization or contamination

conditions that would contribute to low perfusion through the kidney that compromise normal kidney function

chronic heart failure (not enough force to pump blood)

hypotension (decreased BP)

hypovolemia (decreased volume)

hypertension (increased BP)

atherosclerosis (fatty plaque accumulation in BV)

diabetes (sugar coated BV, become hardened)

what consequences occur when the kidneys are deprived of adequate blood flow

kidneys won’t be able to regulate BP and BV which leads to other organs being damaged

kidney then loses mass as it shrinks and hardens (then it becomes nonfunctional)

kidneys require at least _________ of cardiac output going through the flomerulus at one time

25%

prerenal causes of acute renal failure

the kidney is fine but isn’t getting enough oxgenated blood to function

could be caused by cardiac output issue or loss of vascular integrity (meaning kidneys are retaining sodium and then water follows)

25% of cases

renal causes of acute renal failure

failure is due to the kidney itself

could be caused by glomerular disease, tuular disease, or intravascular disease (kidney can’t retain sodium so they aren’t retaining water either)

65% of cases

postrenal causes of acute renal failure

failure is due to the formation of urine normally due to a blockage of urine exiting

10% of cases

difference between prerenal and renal in term of sodium and water

prerenal: kidneys retain sodium so water follows

renal: kidney loses sodium so it loses water

acute renal failure effects

the function of the kidney (prerenal, renal, or postrenal)

which out of the 3 types of acute renal failure is most comonly associated with acute renal failure

acute renal failure (65%)

lab/urinalysis fnding of acute renal failure

sudden decrease in GFR

azotemia

hematuria

proteinuria

electrolyte imbalance

polyuria

oliguria

anuria (depending on cause)

S/S of acute renal failure

polyuria then dehydration

overhydration

edema

heart failure

fatigue

poor appetite

pale skin

why is chronic renal disease sometimes described as “slow and silent”

because it’s not recognizable until about 80-85% of the kidney’s function is lost (because you can function with just one kidney until this point)

approximate percentage of kidney function that must be lost in oder for kidney function to be adversely affected and require treatment in the form of dailysis or a transplant

80-85%

lab findings of chronic renal failure

azotemia

acid base imbalance

electrolyte imbalance

abnormal Ca and P metabolism

anemia

chornic renal failure urinalysis findings

isothenuria (can’t conc urine)

proteinuria

hematuria

increased casts (waxy and broad)

S/S of chronic renal failure

bleeding tendencies

hypertension

weight loss

nausea

vomiting

edema

common locations where renal calculi form

renal calyces (darining tubes)

pelvis

ureter

bladder

most common location of renal calculi formation

renal calyces (draining tubes)

four factors that contribute to the formation of renal calculi

1. hydration status (allows for super saturation)

2. urinary solute status (increased solutes → more likely to precipitate out)

3. changes in urinary pH (acidic/alkaline crystals form)

4. urinary stasis (slow/no movement)

most common constituent of renal calculi

calcium (also oxalate, phosphate, uric acid, and cystine)

all kidney stones have a _______________ core

protein

lab findings/symptoms of renal calculi

severe pain (kidney region radiating forward and donward)

nausea

vomiting

sweating

frequent urge to urinate (dysuria)

oliguria/anuria

hemeturia (b/c some stones are pointy)

dysuria

treatment options for patients with renal calculi

lithotripsy (the surgucal crushing of a stone)

externally using sound waves to break up stones

pain medication to pass tone naturally

calcium oxalate monohydrate stone

calcium oxalate dihydrate stone

uric acid stone

calcium phosphate stone

what are the three types of aminoacidurias

overflow

no threshold

renal aminoacidurias

primary vs secondary causes of aminoacidurias

primary: inherited inborn errors of metabolism or tubular reabsorptive dysfunction

secondary: severe liver disease or generalized renal tubular dysfunction

overflow aminoaciduria

there’s an increase in amino acid excretion so the renal threshold is exceeded so amino acids spill over into the urine

no-threshold aminoaciduria

there’s an increase in amino acid excretion but they aren’t being absrobed at all so everything (meaning AA) ends up in the urine

aminoaciduria

amino acids aren’t breaking down due to missing/defective enzymes

renal aminoaciduria

the levels of amino acids are normal but the tubules are defected causing a lack of absorption so they end up in the urine

cystinuria

an inherited tubular reabsorption problem where cystine (arginine, lysine, and orthotheine) ends up in the urine

cystinosis

an inherited recessive disorder that disrupts the metabolism of cystine so it accumulates in the body/tissues

maple syrup urine disease

an inherited condition where a person lacks enzyme or has defective enzymes so they accumulate leucine, isoleucine and valine

S/S of maple syrup urine disease

severe ketacidosis

seizures

mental development issues

maple syrup urine smell

phenylketonuria

an inherited conditions where a person lacks enzymes or has defective enzymes so phenylalanine accumulates

S/S of phenylketonuria

feeding difficulties

severe mental deficiencies if eating food with phenylalanine

musty/mousy odor

alkaptonuria

an inherited disease due to the lack of an enzyme of defective enzymes so homegenistic acid accumulates in the body

alkaptonuria S/S

darkening of tissues

arthritis due to build up of acid

brown-black color of urine when exposed to air

tyrosinuria

an inherited condition or transient after borth condition due to an immature liver that can’t breakdown tyrosine

S/S of tyrosinuria

spindle/needle like prisms in sheaths, grey-black in color

albinism

a genetic metabolic disorder where a person cant produce melanin or don’t produce normal amounts of melanin

S/S of albanism

no pigmentation in hair, skin, or eyes

sensitive to sunlight

poor eyesight

increased risk of sunbrun or skin cancer

melanuria

a genetic disorder where there’s an overproduction of melanin or melanoma

S/S of melanuria

dark brown/black urine when exposed to air

what hereditary pattern do nearly all aminoaciduria disease have

autosomal recessive