Renal Flashcards
Key functions of the kidneys
Excretion of metabolic waste (urea, creatinine, bilirubin, drugs, hormone metabolites), erythrocyte production via erythropoietin, regulation of water and electrolytes, regulation of BP through RAAS, regulation of acid base (excretion of H ions and reabsorption of bicarbonate), 1,25 dihydroxy vitamins production (calciriol), gluconeogenesis
Renal blood flow
In through renal artery, interlobar artery, arcuate arteries, capillary beds, afferent (glomerular capillaries-filtration), efferent (peritubular capillaries-water, lytes. Substance exchange between blood and filtrate making urine), vasa recta (long efferent arterioles-extend through medullary glomerulus to form juxtaglomerular cells, regulate urine and sodium concentration and volume, reabsorb filtrate to return to systemic circulation), out through renal vein
Filtrate and urine movement through kidney
Bowman’s capsule, proximal tubule, loop of Henle (descending thin, ascending thick), macula densa, distal tubules (8-10 collecting tubules to form), medullary collecting tubule, collecting duct, renal pelvis
Nephron
Glomerulus-glomerular capillaries, fluid is filtered from the blood to form filtrate which enter the tubule
Tubule-tube where filtrate is processed into urine
2 types
Cortical-glomerulus in the outer cortex and tubules that are superficial in the medulla
Juxtaglomerular-glomerulus deep in the cortex that tubes deep into the medulla (vasa recta is here and determines urine concentration)
GFR
Determined by hydrostatic pressure colloid oncotic pressure equals natural filtration pressure
Urine is formed as a result of tubular processing of filtrate aka GFR, absorption of substances from the renal tube, built into the blood excretion of substances from the blood to renal tubes
How to increase GFR
Hormones and artacoids-local angiotensin two- caused by construction of efferent arterioles increase in blood flow increase in GFR
Nitric oxide, prostaglandins, bradykinin- caused by dilating afferent arterioles increasing blood flow increasing GFR
How to decrease GFR
Sympathetic nervous system, nor epinephrine and epinephrine in adrenal medulla-caused by constriction of afferent arterioles decreased blood flow, decreased GFR
Hormones such as endothelin (vascular endothelium)- causes constriction afferent arterioles, decrease blood flow and decreased GFR
Endothelium (fenestrae)in glomerular membrane
Function is to regulate vasomotor tone, homeostasis, trafficking of leukocytes
Glomerular basement membrane (collagen and proteoglycans)
Scaffold supporting the function of the endothelium and podocytes, problems with basement membrane results in albumin leaking into filtrate
Podocyte of glomerular membrane
Filtration slits and slit membrane
The slit serves as a barrier between the foot process to prevent leaking of albumin into the filtrate
Polycystic kidney disease
Etiology- autosomal dominate
Patho- polycystine->epithelium, creates cysts->obstructs renal parenchyma
S/s- progression to CKS
Hemolytic uremic syndrome
Etiology- most common cause of community acquires AKI in kids, due to ecoli 157 toxin-shiga toxin
Patho- abdominal pain, bloody diarrhea, fever, macroangiopathic, hemolytic anemia (shistocytes), thrombocytopenia, microvascular clots clog glomeruli
S/s-progression to CKD
BPH
Etiology- obstruction of urethra
Patho- over distention of bladder leads to hydronephrosis
S/s- overflow incontinence, frequency, UTI, rare AKI/CKD
Chronic glomerular nephritis
Etiology-chronic inflammation (slow to develop), diabetic nephropathy, lupus nephritis
Patho-same as acute and podocyte injury, thickening of basement membrane, and glomerulosclerosis
S/s-n/v, hematuria, proteinuria, HTN, edema, decrease UOP
AKI
Etiology- pre, intrinsic, post renal
Onset is suddenly
S/s-increase in cr, K, phos, BUN, metabolic acidosis, edema, SOB, fatigue, AMS, muddy urine, decline in GFR due to not enough blood at sufficient pressure for perfusion, UOP and clearance of waste products and lytes
Stage 1-creatinine 1.5-1.9 X baseline or greater than or equal to 0.3 mg/dl
Stage 2-creatinine 2-2.9 X baseline
Stage 3- creatinine 3X baseline or use of renal replacement therapy
AKI Patho pre renal
Hypotension, hypovolemia, renal blood flow, renal artery stenosis, abdominal compartment syndrome, usually due to lack of perfusion
AKI Patho intrarenal
Ischemia, acute tubular necrosis, inflammatory conditions, nephrotoxins
AKI Patho post renal
BPH, UTU, urinary stricture, indwelling catheter, urinary obstruction, urine unable to drain causing back up
CKD
Decline in GFR not enough blood to peruse kidneys
Onset insidious
Etiology-chronic injury to nephron, or glomeruli, DM, HTN, glomerulonephritis, PKD, obstruction
Stage 1- severity 90%, GFR greater than 90, mild damage asymptomatic
Stage 2- severity 60-89%, GFR 60-89, mild damage asymptomatic
Stage 3a- severity 30-59%, GFR 45-59, mild to moderate damage but asymptotic
Stage 3b- severity 30-59%, GFR 30-44, some decrease in functional unit, asymptomatic
Stage 4- severity 15-29%, GFR 15-29, severe damage prepare for replacement
Stage 5-severity less than 15%, GFR less than 15, ESRD, kidneys cannot keep up with filtration
Complications of CKD
Osteodystrophy, decreased vitamin D, HTN, HLD, CVD, decreased insulin, increased parathyroid, anemia, impaired platelets, peripheral neuropathy
Nephrolithiasis and urolithiasis
Etiology- masses of crystals, proteins, substrates causes obstruction of urinary tract usually unilateral
Patho-salts in urine precipitate and form crystals that grow (calcium oxalate or phosphate, or uric acid, struvite, mg, ammonium)
S/s- pH of urine greater than 7 if calcium, phosphate or struvite
Less than 5 is urine acid, related to movement or obstruction, pain
Nephrotic syndrome
Etiology- glomerulonephritis, drugs, infection, thromboembolism
Patho-increased permeability through damaged basement membrane
S/s-proteinuria, hypoalbuminemia, edema, HLD, lipiduria
Acute glomerular nephritis
Etiology- post infectious, autoimmune antibodies found in situ, rapidly progressive glomerulonephritis
Patho- depots of IgG and complexes
Kids-group A beta hemolytic strep
Adults-post staph
IgA nephropathy-deposits of IgA (lupus/early diabetic nephropathy)
Membranous glomerulonephritis
Accumulation of macrophages and proliferation of epithelial cells in bowman’s space form crescents and occludes capillary flow
S/s- fatigue, HTN, edema, ascites, proteinuria, hematuria, decreased UOP
Nephritic syndrome
Etiology- infection related and rapidly progressive glomerulonephritis
Patho-inflammation of glomerulus
S/s- hematuria, RBC casts, proteinuria less significant, HTN, oliguria
Age related changes
May hypetrophy as compensatory mechanism due to kidney donation, trauma, disease
Number of nephrons decreases with age beginning at age 40, decreased renal blood flow and GFR
Tubular atrophy-decreased glucose, bicarbonate, sodium reabsorption
Decreased production of vitamin S changes in calcium absorption
Bladder symptoms for common-nephrotic changes and other external causes-hormones, BPH, CVD, position change, diurnal nocturia
Blood labs
Creatinine clearance-reflects GFR, overestimates function
Cystatin C-marker for renal function, measure of serum proteins filters by glomerulus and metabolized by tubules-elevated levels coordinate with decreased GFR, not affected by infection, diet, inflammation, gender, age, race
Urine labs
RBC-glomerular nephritis, trauma, stones
WBC-infection
Casts-coagulated proteins, cellular debris, AKI
RBC casts-tubular of glomerular injury
WBC casts- inflammation
Epithelial casts- tubular injury
Broad waxy- status and tubular injury not a good sign
Bio markers
NGAL-neutrophil gelatinase associated lipocalin-blood and urine
KIM 1-kidney injury molecules 1-urine
IL 18-urine
IGFBIP7- insulin like growth factor binding protein-urine
TIMP2- tissue inhibitor of metalloproteinases 2- urine
Urokinases type plasminigen activator receptor
Proximal tubules
Reabsorbs sodium, chloride, potassium , phosphate, bicarbonate, glucose amino acids, very water permeable
Secretes- H, organic acids, organic bases (metabolic byproducts, bile salts, uric acid, catecholamines)
Controlled by angiotensin II and PTH
Thin descending loop of henle
Reabsorbs small amounts of sodium, highly water permeable
Thin ascending loop of henle
Highly water permeable, dilutes filtrate
Thick ascending loop of henle
Reabsorbs sodium, potassium, calcium, magnesium, bicarbonate, imperator to water, dilutes filtrate
Secretes H ions
Controlled by angiotensin II, PTH
Collecting tubules
Reabsorbs sodium, chloride, calcium, bicarbonate permeable to water, ADH requires
Secretes potassium, K, urea
Controlled by aldosterone, ADH, and ANP
Medullary collection ducts
Reabsorbs urea, water, vasopressin/ADH
Secretes sodium, potassium, H, bicarbonate
Controlled by ADH
