Lecture 6.2: Kidneys Flashcards by Morgan Evans

What do the kidneys do? (2 things)

1) They filter out “everything”
2) They resorb all the “good stuff”

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A&P review:
Describe the A&P of the kidneys

1) High hydrostatic force filters out ions and small molecules in the glomerulus
2) Sodium, water, other ions, glucose, bicarbonate are all resorbed by the renal tubules within the nephron

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Impaired Kidney Perfusion Review:
1) What is impaired kidney perfusion?
2) What does the macula densa do?
3) What do JG cells do?
4) What does nitric oxide do?
5) What does renin do?

1) Any condition where perfusion of the kidney is impaired
2) Senses low-flow state through renal tubules; triggers JG cells to intervene
3) Release nitric oxide + renin
4) Causes the afferent tubule to dilate, increasing blood flow into Bowman’s capsule
5) Angiotensin I is activated and converted into Angiotensin II

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Impaired Kidney Perfusion Review:
What does angiotensin II do? (4 things)

1) Constricts the vessels to raise the blood pressure
2) Enacts release of aldosterone from adrenal glands
3) Acts in the hypothalamus to trigger the thirst response
4) Triggers release of ADH (antidiuretic hormone)

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Impaired Kidney Perfusion Review
1) Why does angiotensin II constricts the vessels to raise the blood pressure?
2) What else acts on the efferent arteriole? (which is disproportionately constricted by comparison to the afferent (remember NO is working upon the afferent tubule)
3) What is the result of this?

1) In an attempt to better perfuse the kidney
2) Vessel constriction
3) Now the Afferent tubule is open wider than the Efferent tubule; this creates a high hydrostatic force, meant to increase filtration

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Impaired Kidney Perfusion Review:
1) What does ADH do? What is the effect?
2) What does aldosterone do?

1) Stimulates the production of aquaporins in the kidney’s collecting ducts; bc the renal medulla is Na rich, water will be resorbed back into the kidney passively
2) Will act in the renal tubules to produce ENAC channels in the collecting ducts (to retain salt); also increases the function of carbonic anhydrase in the collecting ducts.

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Impaired Kidney Perfusion Review
What allows for kidneys to retain salt? What is a byproduct of that?

Aldosterone; also releases K+ when it does so, which has pharmaceutical implications if Aldosterone is blocked

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Impaired Kidney Perfusion Review
1) Aldosterone also increases the function of carbonic anhydrase in the collecting ducts; what does this lead to?
2) What is this clinically important in?
3) What is the end result of all the functions mentioned in impaired kidney perfusion?

1) Increased bicarb production and resorption
2) Dehydrated patients who display a “contraction alkalosis”
3) The GFR is restored + blood volume is bolstered

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1) Define azotemia
2) Define kidney injury
3) When do both of these conditions occur?

1) Elevation of blood urea nitrogen
2) Elevation of creatinine
3) When GFR is low

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There are 3 forms of acute kidney injury; list and describe them

1) Prerenal = lack of blood flow to the kidney
2) Postrenal = obstruction of urine outflow
3) Intrarenal = intrinsic kidney disease

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Post renal AKI:
1) True or false: many of the labs would be similar to prerenal (if you can get them; they may not be releasing much urine).
2) What are the 2 ways to Dx post renal disease?
3) What is the fix?

1) True
2) CT or Ultrasound
3) Removing the obstruction

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1) Why can kidney damage in one place/ structure lead to another?
2) Give 2 examples of this
3) What eventually happens in advanced kidney disease?

1) Because the function of the kidney is so interdependent, one insult leads to another
2) Ex: glomerular damage impairs blood flow through peritubular vasculature, affecting their function
Ex: tubular destruction increases intraglomerular pressure  cytokines + inflammation  glomerular scarring
3) All four regions become impaired

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Acute Tubular Injury/Necrosis (ATN):
1) What is it? What is it the most common cause of?
2) How is it treated?

1) Damage to tubular epithelial cells with acute decline in renal function; most common cause of acute renal failure
2) Supportive care and temporary dialysis
-During this time tubules can regenerate, and kidneys become functional again

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List the signs of ATN, including lab values

1) Electrolyte imbalance, acidosis, uremia
2) Labs: ↓ GFR & ↑ Cr; Urine Micro: Proteinaceous casts & tubular cells
3) Oliguria

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1) What is Acute Interstitial Nephritis (AIN)?
2) What 3 diagnoses fall under this category?

1) Inflammatory cells in the kidney, between tubules.
2) Pyelonephritis, Allergic Nephritis, NSAID Nephropathy

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List some Sx of pyelonephritis

1) Irritative bladder symptoms
2) Dysuria burning in character
3) Urgency
4) Frequency
5) Suprapubic pain
6) Aching in character
7) Systemic sx
8) Fever/chills/sweats/shakes
9) Flank pain CVA Tenderness

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Describe a typical Allergic Nephritis Patient

1) AKI
2) Fever and eosinophilia and a rash
3) Probably just started a new medicine

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1) Define hyaline arteriosclerosis
2) What can it lead to?

1) Sclerosis of small renal arteries and arterioles
2) Progressive & chronic renal damage associated with HTN

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Chronic kidney disease:
1) What is it also called?
2) What are its characteristics? Does the original site of injury make a difference in this?
3) What it the most common pathway to this disease?

1) “End-stage kidney disease”
2) Sclerosed glomeruli, tubules, interstitial and vessels, regardless of original site of injury
3) Glomerular disease → nephrotic syndrome → glomerular sclerosis (chronic glomerulonephritis) → nephron loss → spurious loss of protein

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1) High __________ pressure occurs in Bowman’s capsule
2) There are a few things that DON’T go through Bowman’s capsule in normal physiology; list 2

1) hydrostatic
2) Protein + Large Molecules

1) High hydrostatic pressure occurs in Bowman’s capsule, and water moves from _____________ to Bowman’s space and then to renal tubules  then gets resorbed.
2) What do ions and small molecules do here?

1) capillary lumen
2) Pass through into Bowman’s space and then to renal tubules, then get resorbed

Glomerular Filtration:
1) Capillaries in Bowman’s capsule are mean to do what?
2) What does this mean for its endothelial cells?
3) Define this term & what it allows for

1) to be a filter
2) They’re fenestrated
3) Big “windows” (etymology) that allow water, ions, and small molecules that let things through

Glomerular filtration:
1) Just past the ___________ cells lies the basement membrane.
2) Past this, are the _______________ that wrap their appendages around the fenestrations

1) endothelial
2) podocytes (“foot cell” etymology)

Glomerular filtration:
1) What regulate what gets through?
2) How?

1) The podocytes are what regulate what gets through
2) Fenestrations = 75 nm
Space between podocyte pedicles = 35 nm
Albumen (not supposed to get through) = 15 nm

Glomerular filtration: 1) How is albumen blocked? Explain 2) What does this do to the space?

1) The way that albumen is blocked is by nephrin molecules 2) Makes “nephrin bridges” between foot processes; significantly narrows the space further so that even a molecule as small as albumen cannot get through -They do this by being small and by having a positive charge

What does injury to the podocytes in nephrotic syndrome do? (7 things) What are the late findings

1) Increased permeability 2) Long-standing proteinuria 3) Serum albumin decreased 4) Oncotic pressure drops 5) Edema forms + drop in volume + kidney perfusion decreased 6) Renin-angiotensin system activated 7) Salt and water retention worsens edema “anasarca” Late findings: azotemia, hematuria, HTN

The etiology of hyperlipidemia nephrotic syndrome is unclear, but what are 3 theories?

1) Hypoalbuminemia --> increased synthesis of lipoproteins in the liver 2) Proteinuria --> loss of inhibition of lipoprotein synthesis 3) Impaired breakdown of lipoproteins in the periphery

Nephritic Syndrome Pathology: Describe the chain of events (9 steps)

1) Initial insult within the glomerulus and damage to its cells 2) Epithelial cells of glomerulus are inflamed 3) These cells become increasingly permeable to larger solute 4) Leukocytes are able to infiltrate; passage of blood into the urine 5) Capillary walls are damaged 6) Hemodynamic change occurs in bowman’s space decrease in GFR 7) Azotemia 8) Fluid retention + ischemic kidneys 9) Hypertension as the kidneys attempt to compensate

Nephritic Syndrome 1) How big are normal fenestrations? 2) What now move through the glomerulus because of the inflammation that has occurred? 3) What else gets through?

1) 75nm 2) Leukocytes that would normally be much too large to pass through (25,000nm!) 3) **RBCs** that are only 6,000nm will have no problem getting through; some **albumin** will be able to get through as well

Nephritic Syndrome Pathology: 1) Though RBCs can get through the epithelium, they become deformed passing by what? What does this lead to? 2) Where do the RBCs come do reside? 3) What can be identified on urinalysis?

1) Podocytes; RBC deformity in the urine 2) In the lumen of the renal tubules where they turn to RBC casts 3) Both of these markers

Minimal-Change Disease: 1) Most common cause of nephrotic syndrome in who? 2) Usually seen between ages of ___ and ____ years. 3) Is it benign or a major issue? What is the pathogenesis? 4) More than 90% of cases respond to a short course of ______________ therapy. 5) What else is noteworthy abt this condition?

1) children; insidious development in otherwise healthy kids 2) 1 and 7 3) Relatively benign; pathogenesis poorly described 4) corticosteroid 5) Minimal light microscopic changes with some effacement of foot processes of podocytes

Focal Segmental Glomerulosclerosis (FSGC): 1) What is it the most common cause of? 2) What is it and what does it affect? 3) Is it primary or secondary? 4) What is the response to corticosteroids? 5) What is the prognosis?

1) Most common cause of nephrotic syndrome in adults (can occur in children too) 2) Sclerosis affecting some (but not all) glomeruli and involves only a part of each glomerulus 3) May be primary (idiopathic); often seen as a secondary event with other diseases (HIV, heroin use, IgA nephropathy, maladaption to nephron loss, genetic disorders of podocytes) 4) Usually poor 5) Prognosis is poor: 50% suffer renal failure after 10 yrs

Membranous Nephropathy (MN): 1) What causes it? 2) Describe the characteristics 3) Describe the development & the response to corticosteroids

1) A chronic immune complex induced by antiboides to planted antigens on podocytes 2) Subepithelial immune deposits + spikes of GBM between the immune deposits -Thickening of GBM -Little or no inflammation 3) Insidious development; does not respond well to corticosteroid therapy

Acute Post-Infectious Glomerulonephritis: 1) Caused by what? 2) What is the most common etiology? When? 3) Describe the onset and Sx

1) Immune complex mediated: Glomerular infiltration of immune complexes → damage to glomerular cells and infiltration of leukocytes (neutrophils) 2) Strep Infection; Occurs 1-4 weeks after Group A Strep infection -(also caused by measles mumps, chicken pox, and Hep B & C) 3) Abrupt; “smoky” **tea-colored urine** (oxidation of hemoglobin to methemoglobin resulting in hematuria), mild edema, oliguria, fever, nausea, nephritic syndrome

IgA Nephropathy: 1) What is it the most common form of worldwide? What is it one of the most common causes of? 2) What is the hallmark? 3) Who does it usually affect and when does it occur? 4) What is the course?

1) Primary glomerulonephritis; microscopic and gross hematuria 2) Deposition of IgA in Mesangium 3) Usually children and young adults; 1-2 days after upper respiratory tract as gross hematuria 4) Recurrent, variable course; slow progression to renal failure in 25-50% of patients during 20-year period

Hereditary Nephritis: What causes it? Give 2 examples

Mutations in the genes that encode GBM proteins. 1) Thin basement membrane disease 2) Alport Syndrome

Thin Basement Membrane Diseas What is the most common form of benign familial hematuria with no systemic manifestations?

Thin Basement Membrane Disease

List 3 Sx of Alport Syndrome as a result of type IV collagen differences

Nephritis, nerve deafness, eye abnormalities

Rapidly Progressive (Crescentic) Glomerulonephritis: 1) What type of lesions does it cause? Where? 2) Is it a disease? Explain

1) Proliferative lesions outside capillary loops (made of epithelial cells and macrophages 2) Clinical syndrome (not a single disease)

What are the 3 types of cystic disease of the kidney?

1) Autosomal Dominant (Adult) Polycystic Kidney Disease 2) Autosomal Recessive (Childhood) Polycystic Kidney Disease 3) Medullary Diseases with Cysts

Autosomal Dominant (ADULT) Polycystic Kidney Disease usually presents when? How common is it?

Usually not until the fourth decade of life; accounts for 10 % if all ESRD

(CHILDHOOD) Polycystic Kidney Disease: 1) What is the inheritance? 2) Pathogenesis? 3) How common is it? What is it strongly associated with? 4) What are some Sx?

1) Autosomal recessive inheritance 2) Mutations in the gene encoding fibrocystin 3) Less common than the adult form; liver abnormalities 4) **Kidneys contain small numerous cysts + Oligohydramnios**

Kidney Stones (Renal Calculi) 1) Are they common? Where are they most common? 2) Do they always need Tx?

1) Urinary stones or calculi (urolithiasis) are common; anywhere in urinary tract, most often in the kidney 2) Small stones may be excreted; larger ones may require surgery

List the various types of kidney stones and how common each is

80% -Calcium oxalate Less commonly calcium phosphate 10 % -Struvate 6-7% - Uric acid

Kidney Stones (Renal Calculi) 1) How common are they? Who are they more common in? 2) What are some complications?

1) 5% of everyone during lifetime; men > women, 20-30 years of age 2) Obstruction, pain, infection, or hydronephrosis

Hydronephrosis: 1) What is it? 2) What causes it? 3) Is it acute or chronic? 4) What is a congenital cause? 5) What are some acquired causes?

1) Dilation of the renal pelvis 2) Parenchymal atrophy from urine outflow obstruction 3) May be sudden or slowly developing 4) Urethral atresia 5) Stones, tumors, neurogenic (bladder paralysis), pregnancy related (mild and reversible)

Renal Cell Cancer: 1) Derived from what? 2) How common is it? 3) What are 4 risks?

1) Renal tubular epithelium (in cortex predominately) 2) 80-85% of primary renal malignancies (2-3 % of all adult cancers) 3) Smoking, HTN, obesity, occupational exposure to cadmium

Renal cell cancer: 1) What does prognosis depend on? 2) What are the Txs?

1) Tumor stage, but 5-year survival about 40% (if metastatic, 5%) 2) Radical nephrectomy, but metastases often resistant to chemotherapy and radiation

1) Most common solid (non-hematologic) cancer in children <10 is what? 2) What does it contain? 3) Inheritance?

1) Wilm’s Tumor 2) Variety of cell and tissue components 3) Sporadic or familial (tumorigenesis inherited as an autosomal dominant trait)