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Flashcards in Renal Deck (81):

Kidney Embryology: Pronephros

week 4, then degenerates


Kidney Embryology: Mesonephros

functions as interim kidney for 1st trimester, later contributes to male genital system


Kidney Embryology: Metanephros

permanent, first appears in 5th week of gestation; nephrogenesis continues through 32-36 weeks of gestation
-Ureteric Bud: derived from caudal end of mesonephros; gives rise to ureter, pelvises, calyces, & collecting ducts; fully canlized by 10th week
-Metanephric Mesenchyme: ureteric bud interacts with this tissue; interaction induces differentiation & formation of glomerulus through to distal convoluted tubule
-Abberant interaction b/w these 2 tissues may result in several congential malformations of the kidney


Kidney Embryology: Ureteropelvic Junction

last to canalize, most common site of obstruction (hydronephrosis) in fetus


Potter's Syndrome

-Oligohydramnios, compression of fetus, limb deformities, facial deformities, & pulmonary hypoplasia (cause of death)
-Babies who can't Pee in utero (Potter)
-Causes: ARPKD, posterior urethral valves, bilateral renal agenesis


Horseshoe Kidney

-inferior poles of both kidney's fuse, as they ascend from pelvis during fetal development, horseshoe kidneys get trapped under inferior mesenteric artery & remain low in the abdomen
-kidney functions normally
-associated with Turner syndrome


Multicystic Dysplastic Kidney

-due to abnormal interaction b/w ureteric bud & metanephric mesenchyme
-this leads to a nonfunctional kidney consisting of cysts & connective tissue
-if unilateral (most common), generally asymptomatic w/compensatory hypertrophy of contralateral kidney
-often diagnosed prenatally via ultrasound


Ureters Course

-ureters pass under uterine artery and under ductus deferens (retroperitoneal)
-"water under the bridge" (uterine artery, vas deferens)


Fluid Compartments

Body Weight 40% nonwater, 60% water
-1/3 extracellular, 2/3 intracellular
-1/4 plasma volume, 3/4 interstitial volume
-plasma volume measured by radiolabeled albumin
-extracellular volume measured by inulin
-Osmolarity=290 mOsm/L


Glomerular Filtration Barrier

-responsible for filtration of plasma according to size & net charge
-composed of: fenestrated capillary endothelium (size barrier)
-fused basement membrane w/heparan sulfate (negative charge barrier)
-epithelial layer consisting of podocyte foot processes
-charge barrier is lost in nephrotic syndrome, resulting in albuminuria, hypoproteinemia, generalized edema & hyperlipidemia


Renal Clearance

Cx = (Ux V)/Px = volume of plasma from which the substance is completely cleared per unit time

Cx< GFR; net tubular reabsorption of X
Cx> GFR; net tubular secretion of X
Cx = GFR; no net secretion of reabsorption

V=urine flow rate, Px=plasma concentration
Ux=urine conc. of X, Cx=clearance of X (mL/min)



-Inulin clearance can be used to calculate GFR b/c it is freely filtered & is neither reabsorbed nor secreted
GFR = U(inulin) X V/Pinulin = C inulin
=Kf [(Pgc-Pbs)-(picg-pibs)]
(GC = glomerular capilary; BS = bowmans space)
pi bs normally equals 0
normal GFR = 100 mL/min
Creatinine clearance is approx. measure of GFR, slightly overestimates GFR because creatinine is moderately secreted by the renal tumules
-Incremental reductions in GFR define the stages of chronic kidney disease


Effective Renal Plasma Flow

ERPF can be estimated using PAH clearance b/c it is both filtered & actively secreted in the proximal tubule
-all PAH entering the kidney is excreted
-ERPF = Upah X V/Ppah = Cpah
RBF = RPF/(1-Hct)
ERPF underestimates true RPF by ~10%


Glucose Clearance

-glucose at normal plasma level is completely reabsorbed in proximal tubule by Na+/glucose cotransport
-at plasma glucose of ~160 mg/dL, glucosuria begins (threshold)
-at 350 mg/dL, all transporters are fully saturated Tm
-Glucosuria is an important clinical clue to diabetes mellitus
-normal pregnancy reduces reabsorption of glucose & aa in the proximal tubule, leadign to glucosuria & aminoaciduria


Amino Acid Clearance

-Na+ dependent transporters in proximal tubule reabsorb amino acids


Hartnup's Disease

deficiency of neutral aa (tryptophan) transporter, results in pellagra



affects baroreceptor function; limits reflex bradycardia, which would normally accompany its pressor effects
-helps maintain blood volume & blood pressure



-released from aria in response to inc. volume; may act as a "check" on renin-angiotensin-aldosterone system; relaxes vascular smooth muscle via cGMP, causing inc. GFR, dec. renin



-primarily regulates osmolarity but also responds to low blood volume, which takes precedence over osmolarity



-primarily regulates blood volume, in low volume states, both ADA & aldosterone act to protect blood volume


Juxtaglomerular Apparatus

-consistis of JG cells (modified smooth muscle of afferent arteriole) and the macula densa (NaCl sensor, part of the distal convoluted tubule)
-JG cells secrete renin in response to dec. renal blood pressure, dec. NaCl delivery to distal tubule, & sympathetic tone (beta1)
-JGA defends glomerular filtration rate via renin-angiotensin-aldosterone system
-beta-blockers can decrease BP by inhibiting Beta1-receptors of the JGA, causing dec. renin release



Released by interstitial cells in peritubular capillary bed in response to hypoxia


1-25 (OH)2 vitamin D

-proximal tubule cells convery 25-OH vit D to 1,25 (OH)2 vit D (active form)
-PTH converts it!



-secreted by JG cells in response to dec. renal arterial pressure & inc. renal sympathetic discharge (beta1 effect)



-Paracrine secretion vasodilates the afferent arterioles to inc. GFR
-NSAIDs can cause acute renal failure by inhibiting the renal production of prostaglandins, which keep the afferent arterioles vasodilated to maintain GFR


Renal Tubular Acidosis (RTA)
Type 1 ("distal")

-defect in collecting tubule's ability to excrete H+
-untreated patients have urine pH>5.5
-associated with hypokalemia
-inc. risk for Ca phosphate kidney stones as a result of inc. urine pH and bone resorption


Renal Tubular Acidosis (RTA)
Type 2 ("proximal")

-defect in proximal tubule HCO3- reabsorption
-may be seen with Fanconi's syndrome
-untreated patients typically have urine pH <5.5
-associated with hypokalemia
-inc. risk for hypophosphatemic rickets


Renal Tubular Acidosis (RTA)
Type 3 ("hyperkalemic")

-hypoaldosteronism or lacking of collecting tubule response to aldosterone
-resulting hyperkalemia impairs ammoniagenesis in the proximal tubule, leading to dec. buffering capacity and dec. urine pH


Casts in Urine: RBC

Glomerulonephritis, ischemia, or malignant HTN
-bladder cancer, kidney stones, inc. hematuria, no casts


Casts in Urine

presence of casts indicated that hematuira/pyuria is of renal (vs. bladder) origin


Casts in Urine: WBC

-tubulointersitial inflammation, acute pyelonephritis, transplant rejection
-acute cystitis (pyuria, no casts)


Casts in Urine: Fatty Casts "oval fat bodies"

-nephrotic syndrome


Casts in Urine: Granular

"muddy brown casts"
-acute tubular necrosis


Casts in Urine: Waxy casts

advanced renal disease/chronic renal failure


Casts in Urine: Hyaline casts

Nonspecific, can be a normal findings


Glomerular Disorders: Focal

<50% of glomeruli are involved
Ex: focal segmental glomerulosclerosis


Glomerular Disorders: Diffuse

>50% of glomeruli are involved
Ex. diffuse proliferative glomerulonephritis


Glomerular Disorders: Proliferative

hypercellular glomeruli
Ex: Mesangial proliferative


Glomerular Disorders: Membranous

thickening of glomerular basement membrane
Ex: Membranous nephropathy


Glomerular Disorders: Primary glomerular disease

involves only glomeruli, thus a primary disease of the kidney
Ex: minimal change disease


Glomerular Disorders: Secondary glomerular disease

involves glomeruli & other organs, thus a disease of another organ system, or a systemic disease that has impact on the kidneys
Ex: SLE, diabetic nephropathy


Glomerular Diseases: Nephritic Syndrome

-Acute poststreptococcal glomerulonephritis
-Rapidly Progressive Glomerulonephritis
-Berger's IgA glomerulonephropathy
-Alport syndrome


Glomerular Disorders: Nephrotic Syndrome

-Focal Segmental Glomerulosclerosis
-Membranous Nephropathy
-Minimal Change Disease
-Diabetic Glomerulonephropathy


Glomerular Disorders: Mixed Nephritis/Nephrotic

-Diffuse proliferative glomerulonephritis
-Membranoproliferative glomerulonephritis


Nephrotic Syndrome

-presents with massive proteinuira (>3.5g/day, frothy urine), hyperlipidemia, fatty casts, edema
-associated with thromboembolism (hypercoagulable state due to AT III loss in urine) and inc. risk of infection (loss of Ig)


Focal Segmental Glomerulosclerosis

Nephrotic Syndrome
-LM-segmental sclerosis & hyalinosis
-EM-effacement of foot processes similar to minimal change disease
-most common cause of nephrotic syndrome (adults)
-associated with HIV infection, heroin abuse, massive obesity, interferon treatment, & chronic kidney disease due to congenital absence or surgical removal


Membranous Nephropathy

Nephrotic Syndrome
-LM-diffuse capillary & GBM thickening
-EM-"spike & dome" appearance w/subepithelial deposits
-IF-granular. SLE's nephrotic presentation
-second most common primary nephrotic in adults, can be idiopathic or drugs, infections, SLE, tumor


Minimal Change Disease (Lipoid Nephrosis)

Nephrotic Syndrome
-LM-normal glomeruli
-EM-foot process effacement
-selective loss of albumin, not globulins, caused by GBM polyanion loss
-may be triggered by recent infection or immune stimulus, most common in children
-responds to corticosteroids



Nephrotic Syndrome
-LM- congo red stain shows apple-green birefringence under polarized light
-associated with chronic conditions (multiple myeloma, TB, RA)


Membranoproliferative Glomerulonephritis (MPGN)

Nephrotic Syndrome
Type 1: subendothelial IC deposits with granular IF "tram-track" appearance due to GBM splitting caused by mesangial ingrowth, associated with HBV, HCV
Type 2: intramembranous IC deposits "dense deposits", associated w/ C3 nephritic factor
-also present as nephritic


Diabetic Glomerulonephropathy

Nephrotic Syndrome
-nonenzymatic glycosylation (NEG) of GBM, inc. permeability, thickening
-NEG of efferent arterioles, inc. GBM, cause mesangial expansion
LM-mesangial expansion, GBM thickening, eosinophilic nodular glomerulosclerosis (Kimmelstiel-Wilson lesion)


Nephritic Syndrome

-inflammatory process
-when involves glomeruli, it leads to hematuria & RBC casts in urine
-associated with azotemia, oliguria, HTN (salt retention), & proteinuria (<3.5g/day)


Acute Poststreptococcal Glomerulonephritis

Nephritic Syndrome
-LM-glomeruli enlarged & hypercellular, neutrophils, "lumpy-bumpy" appearance
-EM-sunepithelial immune complex (IC) humps
-IF-granular appearance due to IgG, IgM, and C3 deposition along GBM & mesangium
-most frequent in children
-peripheral & periorbital edema, dark urine, HTN
-resolves spontaneously


Rapidly Progressive (crescentic) Glomerulonephritis (RPGN)

Nephritic Syndrome
-LM & IF- crescent-moon shape. crescents consist of fibrin & plasma proteins (C3b) with glomerular parietal cells, monocytes, & macs
-Several disease:
~Goodpasture's syndrome: type II hypersensitivity; abs to GBM & alveolar basement membrane, linear IF (hematuria/hemoptysis)
~Granulomatosis w/Polyangiitis (Wegener's) (cANCA)
~Microscopic polyangiitis (pANCA)

poor prognosis, rapidly deteriorating renal function (days to weeks)


Diffuse Proliferative Glomerulonephritis (DPGN)

Nephritic Syndrome
-due to SLE or MPGN
-LM- "wire looping" of capillaries
-EM-"subendothelial & sometimes intramembranous IgG-based ICs often with C3 deposition
-most common cause of death in SLE. SLE & MPGN can present as nephrotic syndrome and nephritis syndrome concurrently


Berger's Disease (IgA nephropathy)

Nephritic Syndrome
-related to Henoch-Schonlein purpura
-LM-mesangial proliferation
-EM-mesangial IC deposits
-IF-IgA-based IC deposits in mesangium
-often present/flares with a URI or acute gastroenteritis


Alport Syndrome

Nephritic Syndrome
-mutation in type IV collagen, split basement membrane
-glomerulonephritis, deafness, & less commonly, eye problems


Types of Kidney Stones

1. Ca
2. Ammonium Magnesium Phosphate "struvite"
3. Uric Acid
4. Cystine


Kidney Stones: Ca

inc. pH (calcium phosphate), dec. pH (calcium oxalate) percipitates
-radiopaque on x-ray
-conditions that cause hypercalcemia (cancer, inc. PTH) can cause hypercalciuria & stones
-oxalate crystals can result from ethylene glycol (antifreeze) or vit. C abuse
-Treatment: thiazides, citrate
-most common presentation: calcium oxalate stone in patient w/hypercalciuria & normocalcemia


Kidney Stones: Ammonium Magnesium Phosphate "struvite"

precipitates at inc. pH
radiopaque on x-ray
-caused by infection w/urease-postitve bugs (proteus mirabilis, staphlococcus, klebsiella) that hydrolyze urea to ammonia, urine alkalinization
-can form staghorn calculi that can be nidus for UTIs


Kidney Stones: Uric Acid

5%, precipitates with dec. pH
-radiolucent with x-ray
-visible on CT & ultrasound
-strong association with hyperuricemia (gout), often seen in diseases with inc. cell turnover like leukemia
Treat: alkalization of urine


Kidney Stones: Cystine

1%, precipitates with dec. pH
-radiopaque on x-ray
-most often secondary to cystinuria
-hexagonal crystals
-treat with alkalinization of urine



-back-up of urine into the kidney, can be caused by urinary tract obstruction or vesicoureteral reflex.
-causes dilation of renal pelvis & calyces proximal to obstruction
-may result in parenchymal thinning in chronic, severe cases


Renal Cell Carcinoma

-Originates from proximal tubule cells, polygonal clear cells filled with accumulated lipids & carbohydrates
-most common in men 50-70, inc. incidence with smoking/obesity
-manifests clinically with hematuria, palpable mass, secondary polycythemia, flank pain, fever, & weight loss
-invades renal vein then IVC & spreads hematogenously
-metastasizes to lung & bone
-most common renal malignancy
-associated with gene deletion on chromosome 3 (deletion may be sporadic or inherited as von Hippel-Lindau syndrome)
-Associated with paraneoplastic syndromes (ectopic EPO, ACTH, PTHrP)
-"silent" cancer b/c in retroperitoneum, commonly presents as a metastatic neoplasm
Treatment: resection if local disease, resistant to convential chemo and radiation


Wilms' Tumor (Nephroblastoma)

-most common renal mallignancy of early childhood (2-4)
-contains embryonic glomerular structures
-presents with huge, palpable flank mass and/or hematuria
-deletion of tumor suppressor gene WTI on chromosome 11
-may be part of Beckwith-Wiedemann syndrome or WARG complex: Wilm's tumor, Aniridia, Genitourinary malformation, & mental retardation


Transitional Cell Carcinoma

-most common tumor of renal tract system (can occur in renal calyces, renal pelvis, ureters, bladder)
-painless hematuria (no casts) suggests bladder cancer
-associated with problems in your Pee SAC:
Phenacetin, Smoking, Aniline Dyes, and Cyclophosphamide


Acute Pyelonephritis

-affects cortex with relative sparing of glomeruli/vessels
-presents w/fever, costovertebral angle tenderness, nausea, & vomiting
-white cell casts in urine


Chronic Pyelonephritis

-result of recurrent episodes of acute pyelonephritis
-typically requires predisposition to infection such as vesicoureteral reflux or chronically obstructing kidney stones
-course, asymmetric corticomedullary scarring, blunted calyx
-tubules can contain eosinophilic casts (thyroidization of kidney)


Drug-Induced Interstitial Nephritis (tubulointerstitial nephritis)

-acute interstitial renal inflammation
-pyuria (classically eosinophils) & azotemia occurring after administration of drugs that act as haptens, inducing hypersensitivity
-nephritis typically occurs 1-2 weeks after certain drugs (diuretics, penicillin derivatives, sulfonamides, rifampin), but can occur months after starting NSAIDS
-associated with fever, rash, hematuria, & costovertebral angle tenderness, but can be asymptomatic


Diffuse Cortical Necrosis

-acute generalized cortical infarction of both kidneys
-likely due to a combination of vasospasm & DIC
-associated with obstetric catastrophes (abrupto placentae) & septic shock


Acute Tubular Necrosis

-most common cause of intrinsic renal failure
-self-reversible is some cases, but can be fatal if left untreated
-death most often occurs during initial oliguric phase
3 Stages:
1) Inciting Event
2) Maintencance Phase - oliguric; lasts 1-3 weeks, risk of hyperkalemia
3) recovery phase-polyuric; BUN & serum creatinine fall; risk of hypokalemia
-associated with renal ischemia (shock, sepsis), crush injury (myoglobinuria), drugs, toxins
-key findings: granular "muddy brown" casts


Renal Papillary Necrosis

-sloughing of renal papillae, gross hematuria & proteinuria, may be triggered by a recent infection or immune stimulus, associated with:
-diabetes mellitus
-acute pyelonephritis
-chronic phenacetin use (acetaminophen is phenacetin derivative)
-sickle cell anemia & trait


Acute Renal Failure (acute kidney injury)

-in normal nephron, BUN is reabsorbed (for countercurrent multiplication), but creatinine is not
-acute renal failure is defined as an abrupt decline in renal failure with inc. creatinine & inc. BUN over a period of several days


Prerenal Azotemia

Acute Renal Failure (acute kidney injury)
-as a reslut of dec. RBF (hypotension), dec. GFR
-Na+/H2O & urea retained by kidney in an attempt to conserve volume, so BUN/creatinine ration inc.


Intrinsic Renal Failure

Acute Renal Failure (acute kidney injury)
-generally due to acute tubular necrosis or ischemia/toxins; less commonly due to acute glomerulonephritis (RPGN)
-patchy necrosis leads to debris obstructing tubule & fluid backflow across necrotic tubule, dec. GFR
-urine has epithelial/granular casts
-BUN reabsorption is impaired, dec. BUN/creatinine ration


Postrenal Azotemia

Acute Renal Failure (acute kidney injury)
-due to outflow obstruction (stones, BPH, neoplasia, congenital anomalies)
-develops only with bilateral obstruction


Consequences of Renal Failure

-inability to make urine & excrete nitrogenous wastes
-Acute (ATN) & Chronic (HTN, diabetes)
-Na+/H2O retention (CHF, pulmonary edema, HTN)
-metabolic acidosis
-uremia-clinical syndrome marked by inc. BUN & inc. creatinine (nausea, anorexia, pericarditis, asterixis, encephalopathy, platelet dysfunction)
-anemia (failure of erythropoietin production)
-renal osteodystrophy
-dyslipidemia (especially inc. triglycerides)
-growth retardation & developmental delay (in kids)


Renal Osteodystrophy

-failure of vit D hydroxylation, hypocalcemia, & hyperphosphatemia, secondary hyperparathyroidism
-hyperphosphatemia also independently dec. serum Ca2+ by causing tissue calcifications, whereas dec. 1,25 (OH) vit D, dec. intestinal Ca2+ absorption
-causes subperiosteal thinning of bones


Renal Cysts: ADPKD

-formerly adult polycystic kidney disease
-multiple large, bilateral cysts that ultimately destroy the kidney parenchyma
-present with flank pain, hematuria, HTN, urinary infection, progressive renal failure
-Autosomal Dominant mutation in PKD1 or PKD2, death from complications of chronic kidney disease or HTN (caused by inc. renin production)
-associated with berry aneurysms, mitral valve prolapse, benin hepatic cysts


Renal Cysts: ARPKD

-formerly infantile polycysitc kidney disease
-infantile presentation in parenchymal
-autosomal recessive
-associated with congential hepatic fibrosis
-sig. renal failure in utero can lead to Potter's syndrome
-concerns beyond neonatal period include HTN, portal HTN, & progressive renal insufficiency


Medullary Cystic Disease

-inherited disease causing tubulointerstitial fibrosis & progressive renal insufficiency with inability to concentrate urine
-medullary cysts usually not visualized; shrunken kidneys on ultrasound
-poor prognosis