Renal

• Outline Renal Disease

  glomerulonephritis

  • nephrotic - mild
  • nephritic - severe

  tubulointerstitial disorders

  • pyelonephritis - infective
  • Interstitial nephritis - non infective

  Urinary Calculi - nephrolithiasis

  renal failure - acute, chronic, congenital
• glomerular disease = glomerulonephritis

  Affect primarily the renal corpuscle where you have glomerular capsule/ capillary

  • Part of nephron responsible for filtration
• descriptions of glomerulonephritis

  • acute - benign, resolves quickly
  • rapidly progress
  • chronic - progress, dialysis, new kidney
  • diffuse (throughout kidney) vs focal (only portion of kidney)
• Types of glomerular change

  • minimal change - changes in podocytes
  • proliferative
  • membranoproliferative
  • diffuse proliferative
• Filtration barrier/membrane

  filtration: capillary -> bowmans capsule/ glomerular capsule

  3 layers

  • glomerular endothelial cells = simple squamous epi
  • basement membrane = lots of proteins = block movemet of large negative proteins
  • Podocytes slit membrane blocks medium size protein
  • menengial cells - sit b/w capillaries, contract reduce SA to regulate BP -> GFR
• Pathology of glomerulonephritis

  Due to: primary immune-mediated (70%), infection hep b + c, streptococcus, tumors
• immune-mediated glomerulonephritis

  due to: antibodies target glomerular capillary for destruction

  • seen with antibodies/antigen complexes that as move through blood stream, try to pass filter; when lodge in glomerular capsule filter trigger inflammation
  • involve type II hypersensitivity - involves Ab that target filter/glomeruli for destruction (good pastures)
  • involve type III hypersensitivity: Ab-Ag complexes large and lodge in glomeruli filter
• Alter glomerular filter

  1. Immune complexes (antibody-antigen) trigger inflammation: Ab-Ag lodge in filter
  2. Mesengial cell damage leads to decreased regulation of glomerular capillary blood pressure / GFR
  3. Exposure of basement membrane leads to platelet aggregation and microthrombi (obstruction) - expose BM -> collagen expose -> platelets like to attach to collagen
• glomerular disease = glomeronephritis

  Results in altered filtration

  • altered filtrate (what makes it through filter) then plasma concentration
  • Alters rate of glomerulation filtration (GFR) - change H₂O vol + electrolytes
  • Too slow- build up waste / too fast- flush out things may need
  • Most common cause of renal failure
• change in filter in glomerulonephritis

  • end up with more obstruction, areas with clots, or create holes (allows thing to pass that normally can't
• Nephrotic syndrome - benign, tends to resolve


  filtrate change

  • proteinuria = loss of protein (can't be reabsorbed = lost in urine)

  plasma change

  hypoalbumemia (low albumin)

  • low plasma proteins = low osmotic pressure (fluid moves from plasma -> interstitial, but not back in) = systemic edema
  • most obvious in ankles/ascites
• Liver response in nephrotic syndrome

  • Increased protein & lipid synthesis
  • Hyperlipidemia (more lipoproteins)
  • Low clotting factors
  • Low globulins (immunosuppression)
• Renal response in nephrotic syndrome

  respond to movement plasma -> interstitial = decrease blood volume

  Kidneys retain fluid + increase sys. BP , but fluid moves to interstitial b/c no proteins to maintain osmotic pressure -> exacerbates Systemic edema
• Nephritic syndrome - more severe, rapidly progress, deadly


  inflammation results in scar tissue disposition (clog filter)

  • decrease blood filtration -> reduced GFR
• Nephritic syndrome

  filtrate change

  • decreased urine output (oliguria) -> if not getting rid of urine, not getting rid of waste
  • blood in urine (hematuria)

  plasma change

  • not filtering -> water retention -> increase blood volume -> increase systemic BP (hypertension)
  • nitrogen waste retention (azotemia) - increase ammonia/urea in blood
  • low plasma protein variable - either lose them or filter blocked: depends on differences in damage to glomeruli filter (intact BM prevents passage of proteins with negative change but not RBCs)
• Nephritic syndrome is associated with proliferative -> progressive glomerulonephritis (GN)
• Tubulointerstitial disorders

  Involve damage to renal tubules and peritubular capillaries
• Tubulointerstitial disorders interfere with

  • reabsorption - interfere with reabsorption of sodium/water = results in loss
  • secretion (normally results in excretion) - retain hydrogen ions ( low pH = acidosis) + potassium
• Types of tubulointerstitial disorders

  • Pyelonephritis
  • interstitial nephritis
• Pyelonephritis

  due to bacteria (two ways to get into kidney)

  • Descending infection (come in through blood/renal artery)
  • Ascending infection (90% - comes from urinary tract)

  more common in female due to shorter urethra
• Pyelonephritis

  • Infective agent can be E.coli (from feces)
  • moves from urinary tract -> bladder -> ureters -> kidney
  • common in males over 40 due to prostate enlargement -> harder to force fluid through urethra -> inadequate bladder emptying -> bacteria easily crawls up urethra
  • also common pregnant women/ppl with bladder stones
• Pyelonephritis also due to vesicoureteral reflux - congenital disease resulting in dilated ureter and reflux of urine to ureter
• Acute pyelonephritis

  • bacterial can lead to inflammation, suppuration and necrosis
  • Signs include pain, chills, fever, pyuria (pus in urine), bacteriuria (bacteria in urine)
  • Treated with antibiotics
• Chronic pyelonephritis


  • Associated with people that have congenital vesicoureteral reflux, constantly refluxing bacteria and leading to multiple acute infections and scarring
  • Can also be due to obstruction from stones
  • Signs include asymptomatic deterioration and scar tissue (50% destruction of nephrons)
  • Can lead to renal failure
• Interstitial nephritis

  Caused by:

  non-infective agents,

  toxins (nephrotoxins) - metals, solvents, therapeutic agents: antibodies

  
  

  toxic because of huge blood supply to kidney - 20% of cardiac output flows thru kidney = increased exposure (has to pass through here)
• Urinary Caliculi = nephrolithiasis


  Formation of stones that can block urinary tract

  form in places where urine can pool - allow calcium to aggregate + form stones

  
  

  occur in:

  renal pelvis but gets stuck in ureter

  bladder but gets stuck in urethra
• Urinary calculi = nephrolithiasis

  • Urinary stones occur in 1 in 100 cadavers
  • problem 1 in 1000 (when try to pass)
• Composition of urinary stones

  • Calcium ( mostly) + combines with Oxalate, Phosphate, Urate
• signs of urinary caniculi = nephrolithiasis

  • Can be asymptomatic, unless trying to pass and get stuck (obstruction)- more common in males due to narrower urethra
  • increased risk of infection
  • cause pain (renal colic)
  • cause hematuria (blood in urine)
• Treatment of urinary calculi

  1. change urine pH (acidic pH = dissolves stones)

  2. Flush out (increased urine volume to push out stones)

  3. Remove stones (lithotripsy or surgery)
• Renal Failure

  • Prerenal - source/cause is blood supply
  • can come from Ag-Ab (glomerulonephritis) or toxins (tubulointerstitial disease)
  • due to blood flow/BP - low blood flow/BP result in ischemia (decreased O2 = death of nephrons) -> decreased GFR (build up of waste) or high BP (hypertension) -> increased GFR
  • Intrinsic - juxtaglomerular (myogenic) triggers afferent artery to vasoconstriction but can't forever, allowing more blood flow to glomerular capillary -> increased glomerular cap BP -> increased GFR (elevated proteins in urine/cause hole/damage to filter)
• renal failure - Post renal

  source is urinary obstruction - cause urine to back up, creating back pressure causing cells to be inflamed

  obstruct urine excretion
• Renal failure - renal

  kidney is cause - changes within kidney due to increased nephron destruction
• Acute renal failure

  • Usually due to ischemia
  • results in rapid drop in urine output - <400ml/day (25% of normal), anuria (no output - stopped producing urine)
  • see acute tubular necrosis (destruction of nephrons)
  • can recover but resolves over weeks
• chronic renal failure

  • progressive nephron destruction
  • signs - (50-70% nephrons destroyed)
• Signs of renal failure

  • Decreased filtration/GFR (destruction of renal tubules/peritubular capillaries)
  • Uremia - accumulation of nitrogen waste (urea/ammonia), results in nausea, vomiting, no appetite, pruitus, pericarditis, uremic encephalopathy
  • water reabsorption - Reabsorption/secretion: water loss, sodium loss (hypotonic- fluid moves into cells -> cell swell + burst)
  • hydrogen ion retention = low pH (acidic) = acidosis
• Signs of Renal Failure

  
  

  End stage renal failure= Anuria (stopped producing urine) - retain water and increase BP = systemic edema

  
  

  changes in blood/urine

  • blood elevated: creatine (waste product) / blood, urea, nitrogen (BUN)
  • Urine: low specific gravity - flush out large volumes of dilute urine / see protein, blood bacteria
• Clearance tests - Determine kidney function

  • give you waste product
  • normal kidney clears it
  • failure - kidney clears in prolonged time
  • if kidney failing stop producing erythropoietin -> anemia
• Hemodialysis

  1. Take patient's blood, flow through hemodialyser, filter out waste and return electrolytes/proteins

  2. Takes 3-4 hours, 3 times per week

  3. Longer treatment time for larger patients
• Peritoneal dialysis

  1. Use same mechanism but filter used in peritoneal cavity

  2. Takes 4-6 hours

  3. Risk of infection