Patho Renal

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Waste products excreted by the kidneys

Urea, Creatinine, Bilirubin, Drugs, and Hormone Metabolites

Kidneys Regulate?

Water and Electrolyte Balance

Kidneys Regulate BP Through?

RAAS

Kidneys Regulate Acid-Base Balance Through?

Excretion of H+ and Reabsorption of Bicarbonate

Kidneys Regulate Erythrocyte Production By?

Erythropoietin Production

Kidneys Regulate

1,25-Dihydroxy Vitamin Production

Kidneys Regulate

Gluconeogenesis

Outer Portion of Kidneys

Cortex

Inner Portion of the Kidneys

Medulla

Organized tissue in the medulla that communicates with the renal pelvis

Renal Pyramids

Collect urine made by the kidneys and lead to the renal pelvis -> ureters -> bladder

Minor and Major Calyx

The functional unit of the kidney that makes urine located in the cortex and medulla (cannot be regenerated)

Nephrons

Tuft of glomerular capillaries where fluid is filtered from the blood -> creates a filtrate which enters the tubule

Glomerulus

Tube in which filtrate is processed into urine

Tubule

Network of capillaries in the renal cortex covered by epithelium called Bowman’s Capsule. Blood is filtered and fluid is collected in Bowman’s Capsule. Vascular tone of afferent and efferent arterioles control rate of filtration.

Glomerulus

Bowman’s Capsule -> proximal tubule -> loop of Henle [descending (thin) and ascending (thick) limbs] -> collecting tubules -> 8-10 collecting tubules combine to medullary collecting tubule -> collecting duct -> renal pelvis

The Tubule System

Glomerulus in the outer cortex and tubules that only go a short way into the medulla

Cortical Nephron

Glomerulus deep in the cortex with tubules that go a long distance into the medulla

Juxtaglomerular Nephron

These nephrons have specialized vasculature surrounding their periorbital capillaries (vasa recta) which absorb fluid into systemic concentration determining the urine concentration

Juxtaglomerular Nephron

Renal Artery branches into

Interlobar Artery and Arcuate Arteries

Capillary Beds Are Comprised of

Afferent and Efferent (Vasa Recta)

Function of Afferent Arterioles -> Glomerular Capillaries

Where Filtration Occurs

Where water, electrolytes and substances exchange between blood and filtrate making urine

Function of Arterioles-> Peritubular Capillaries

Adjusting the resistance of the afferent and efferent arterioles controles hydrostatic pressure in the glomerulus->

Controls Glomerular Filtration Rate (GFR) = rate which blood flows through the kidneys

Long efferent arterioles that extend the length of the medullary glomerulus and form the Juxtaglomerular cells

Vasa Recta

Regulate urine and serum concentration and volume; reabsorb filtrate to return to systemic circulation

Vasa Recta

Function of Urine Formation

Glomerular Filtration, Reabsorption or Substances from the Renal Tubules into the Blood, Excretion of Substances from the blood into the Renal Tubules

Movement of fluid and substance from blood -> glomerular capillaries-> Bowman’s Capsule

Glomerular Filtration

Filtered Fluid containing little protein or cellular elements if the capsule is intact, and has less calcium and fatty acids than blood

Filtrate

Sum of hydrostatic and colloid osmotic pressures across the glomerular membrane (net filtration pressure)

Glomerular Filtration Rate

Glomerular Filtration Membrane is Comprised of

Endothelium (Fenestrae), Basement Membrane (Collagen and Proteoglycans), and Podocyte (Filtration Slits/Slit Membranes)

Ways to Decrease GFR

Increase Bowman’s Capsule Hydrostatic Pressure (obstruction of urinary tract-kidney stone), Increase Glomerular Capillary Colloid Osmotic Pressure (high protein intake and hyperglycemia)

Ways to Increase GFR

Increase Glomerular Capillary Hydrostatic Pressure, Increase Intravascular Volume or MAP, Dilation of Afferent Arterioles = more blood flow, Constrict Efferent Arterioles = slower flow and greater blood volume

Ways to Decrease GFR

Sympathetic Nervous System (Epi and Norepi both decrease blood flow by constricting afferent arterioles)

Ways to Decrease GFR

Hormones (Endothelin-constrict afferent arterioles->decrease blood flow)

Ways to Increase GFR

Local Angiotensin II (constrict efferent arterioles increasing blood flow)

Ways to Increase GFR

Nitric Oxide, Prostaglandin, Bradykinin (dilate afferent arterioles increasing blood flow

Macula densa cells in the distal tubules sense sodium and decreased blood flow-> signal to Juxtaglomerular cells to produce renin-> RAAS system

Juxtaglomerular Apparatus

Reabsorption of sodium, potassium, phosphorus, bicarbonate, glucose, amino acids. Very permeable to water.

Proximal Tubule

Secretes H+, organic acids, organic bases (metabolic byproducts, bile salts, uric acids, catecholamines)

Proximal Tubule

Controlled by Angiotensin II (increase Na+ and water absorption) and parathyroid hormone (decreased phosphorus reabsorption)

Proximal Tubule

Reabsorption of small amounts of Na+, highly permeable to water, creates highly concentrated filtrate, no secretion

Thin Descending Loop of Henle

Reabsorption of sodium, potassium, calcium, magnesium, bicarbonate. Impermeable to water. Dilutes filtrate. Secretes H+. Controls Angiotensin II (NaCl reabsorption and H+ secretion). Parathyroid hormone (Calcium reabsorption).

Thick Ascending Loop of Henle

Reabsorption of sodium, calcium, bicarbonate. Permeable to water (antidiuretic hormone required). Secretes potassium, H+, urea. Controls Aldosterone (increase NaCl and K+ secretion), Vasopressin/ADH (increase water reabsorption), ANP (decreases Na reabsorption)

Collecting Tubules

Reabsorp of urea

Reabsorption of urea, water if vasopressin/ADH. Secretion or Reabsorption of sodium, potassium, H+, bicarbonate. Controls vasopressin/ADH (increase water reabsorption)

Osmolarity of medullary interstitum

1200 Osmo/L

Osmolarity of interstitial fluid

300 Osmo/L

Reflects GFR, estimate that overestimates function

Creatinine Clearance

Blood x 1 and 24 hr urine, normal level varies by age and gender. Useful if kidney function is stable. Picks up small, significant early changes in serum creatinine

Creatinine Clearance

Marker of kidney function, measure of serum protein filtered by glomerulus and metabolized by tubules

Cystatin C

Elevated level correlates with decreased GFR. Not affected by infection, diet, inflammation, gender, age, or race.

Cystatin C

RBCs in Urine indicate?

Glomerulonephritis, trauma, kidney stones; tubular or glomeruli injury

WBCs in Urine Indicate?

Infection and Inflammation

Casts in Urine Indicate?

Coagulated Proteins

Cellular Debris in Urine Indicate?

AKI

Epithelial in Urine Indicate?

Tubular Injury

Broad Waxy Cells in Urine indicate?

Stasis and Tubular Injury (poor sign)

Neutrophil gelatinase-associated lipocalin (plasma, urine)

NGAL

Kidney Injury Molecule I (urine)

KIM I

Interleukin-I8 (urine)

IL-I8

Insulin-like growth factor-binding protein (urine)

IGF BIP7

Tissue inhibitor of metalloproteinases-2 (urine)

TIMP-2

As Kidneys Age Renal Cells May?

Hypertrophy

As number of nephrons decrease with age

Decreases renal blood flow and GFR

As tubular atrophy occurs with age

Decreases glucose, bicarb, and sodium reabsorption

Decrease production of Vit D by kidneys with aging

Changes intestinal Ca absorption

Bladder symptoms are more common with aging kidneys causing

Nephrotic/external changes: hormone changes, prostate hypertrophy, CV disease

Masses of crystals, protein or substances that cause obstruction of urinate tract (typically unilateral)

Nephrolithiasis & Urolithiasis

Pathogenesis: salts in urine precipitate and form crystals that grow (aggregate). Manifestations related to movement or obstruction.

Nephrolithiasis & Urolithiasis

Classified according to primary salt that makes up the stone: calcium oxalate or phosphate, uric acid, struvite - magnesium, ammonium, phosphate

Nephrolithiasis & Urolithiasis

pH of urine can promote stones (alkaline pH > 7.0 calcium, phosphate, and stuvite; acidic pH < 5.0 uric acid)

Nephrolithiasis & Urolithiasis

Injury to endothelium, basement membrane, podocytes. Hallmark = altered permeability and selectivity. Manifestations- Proteinuria, hematuria, urinary sediment, oliguria, edema, hypertension, azotemia.

Glomerular Diseases

Inflammatory Glomerular Disease

Circulating antigen-antibody complexes deposit in glomerulus-> antibodies react with antigens in the glomerulus (in situ)-> Antibodies degrade glomerular capillary (basement membrane)-> Activation of immune/inflammatory response-> More injury to basement membrane-> Decreased GFR, increased membrane permeability, cell proliferation, sclerosis, thickened BM.

Post-infectious: deposits of IgG and complement complexes -> Kids: post group A. strep; Adults: post-Staph

Acute Glomerulonephritis

Deposits of IgA -> 24-48 hrs post URI and viral GI infection; related to lupus nephritis or early diabetic nephropathy.

IgA Nephropathy

Autoimmune, Antibodies formed in situ

Membranous Glomerulonephritis

Accumulation of macrophages and proliferation of epithelial cells in Bowman’s space, forms crescents and occludes glomerular capillary blood flow (3 types, diagnose and treat early or -> CKD and transplant)

Rapidly Progressive Glomerulonephritis

Typically associated with chronic inflammatory process. Slow developing until develop nephrotic syndrome -> ESRD.

Chronic Glomerulonephritis

Associated with: Diabetic Nephropathy - podocyte injury, thickening of basement membrane and Glomerulosclerosis; Lupus Nephritis - immune complex deposition, basement membrane damage.

Chronic Glomerulonephritis

Protein (albumin) in urine

Proteinuria

Normal protein level in urine

</= 150mg/d

Significant protein level in urine

300-500mg/d

Nephrotic urine protein level

>3g/day

>3.5g/day protein in urine

Glomerular Disease

1-2g/day protein in urine

Tubular Disease

Albumin-Creatinine ratio can substitute for

24-hour urine

Presents with significant Proteinuria. Associated with chronic glomerulonephritis, drugs, and infections. Manifestations: hypoalbuminemia, edema, hyperlipidemia, and lipiduria.

Nephrotic Syndrome

Presents as hematuria and RBC casts (Proteinuria but less significant). Associated with infection related and rapidly progressive glomerulnephritis. Manifestations: HTN, oliguruia.

Nephritic Syndrome

Sudden decline in GFR, U/O and clearance of waste products and electrolytes

AKI

1.5-1.9 x baseline Cr or >/= 0.3 mg/dL increase

Stage I AKI

2-2.9 x baseline Cr

Stage 2 AKI

3.0 x baseline Cr or use of renal replacement therapy

Stage 3 AKI

Inadequate perfusion (not enough blood at sufficient pressure to allow filtering). Manifestations: hypotension and hypovolemia. Renal blood flow: renal aretery stenosis, abdominal compartment syndrome. Common cause of of AKI. Fe(na): <1% pre-renal AKI.

Pre-Renal

Cellular damage (injury to the cells that make filtering possible). Inflammatory conditions, acute tubular necrosis (ATN), nephrotixins. Most common cause of ATN from ischemia. Fe(na): >1% intrinsic or post-renal AKI.

Renal/Intrinsic

Obstruction (urine is unable to drain and system backs up). Fe(na): >1% intrinsic or post-renal AKI.

Post-Renal

Elevated Cr and oliguria - important feature of AKI. Electolyte abnormalities: K, Phos, BUN. Metabolic Acidosis. Edema, dyspnea -> F/O. Fatigue, AMS. Brown urine?

Manifestions of AKI

No specific symptoms, but kidney function can slowly decline

Stage 1-3

Kidney function is very low, and treatment for kidney failure may be neeed soon.

Stage 4

Kidneys can no longer keep up with removing waste products and extra water. This is called kidney failure. Although there is no cure, treatment options are available.

Stage 5

100

Reabsorption of urea and water (vasopressin/ADH). Secrete or Reabsorb - Na, K, H+, bicarbonate. Controlled by - vasopressin/ADH (increase H2O reabsorption)

Medullary Collecting Ducts

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