Nephrology Flashcards
glomerular disorders
-Glomerulonephritis
-Nephritic/Nephrotic Syndromes
-Diabetic Nephropathy
components of nephrone
2 types of nephrons
-Juxtamedullary (left):
~ 15% of nephrons
-starts deeper and goes deeper in (inner medula)
-different/better concentration gradient
-uses more energy but concentrates heavily
-Cortical (right):
~ 85% of nephrons
-more shallow
-dont memorize numbers
roles of nephrons
-Juxtamedulary
-Primarily for urine concentration
-Reabsorb higher proportion of filtrate
-High use of energy
-Cortical
-Lower use of energy
-Less efficient at conserving fluid
-Blood flow can be directed to conserve fluid or energy
renal corpuscle
-podocytes- line the capillary -> change how much we filter
-damaged podocytes -> proteins in urine, cells in urine, glucose
filtration at the glomerular level
-Filtrate must pass through the:
-1. Fenestrated capillary membrane
-2. Glomerular basement membrane
-3. Podocyte foot processes
transmembrane transport mechanisms
-7 basic mechanisms for transmembrane transport of solutes
-1. Convective flow in which dissolved solutes are “dragged” by bulk water flow
-2. Simple diffusion of lipophilic solute across the membrane
-3. Diffusion of solute through a pore
-4. Transport of solute by carrier protein down electrochemical gradient
-5. transport of solute by carrier protein against an electrochemical gradient with ATP hydrolysis providing driving force
-6,7. Co-transport and countertransport, respectively, of solutes, with one solute traveling uphill against an electrochemical gradient and the other solute traveling down an electrochemical gradient
-active or passive
-NOT ON TEST
common nomenclature for tubular segments
-proximal tubule- prox convoluted tubule and prox straight tubule
-loop of henle- descending thin, ascending thin, and thick ascending limb of loop of henle
-distal tubule- distal convoluted tubule
-distal nephron- distal tubule, connecting tubule, cortical collecting duct
-medullary collecting duct- outer medullary collecting duct and inner medullary collecting duct
renal osmolarity
-Keep in mind that the interstitial space makes up a fraction of the actual kidney… but for demonstration purposes…
-active transport sets up concentration gradient for passive transport
-collecting duct channels are open in presence of ADH
-in presence of ADH -> H2O diffuses out of tubule and we pee concentrated urine
stepwise approach to renal filtration
-afferent arterial going into the glomulus
-efferent coming out
-all the water that leaves the tubule is reabsorbed by the afferent arteriole -> counter current multiplier
if we laid renal function out on a straight line and graphed its function
-look at the ADH and without ADH
-Cr kidney marker
kidney pain
-stretch of the capsule from inflammation
feedback loop for aldosterone secretion
-Feedback mechanism regulating aldosterone secretion
-dashed arrow indicates inhibition
-Renin is a proteolytic enzyme produced from a larger protein, prorenin
-Renin is excreted by the juxtaglomerular cells of the kidney in response to decreases in renal perfusion pressure and reflex increases in renal nerve discharge
-Once in the circulation, renin acts on angiotensinogen, to form angiotensin I, a decapeptide
-In the lung and elsewhere, angiotensin I is converted by angiotensin-converting enzyme (ACE) to angiotensin II, an octapeptide
-Angiotensin II binds to zona glomerulosa cell membrane receptors and stimulates synthesis and secretion of aldosterone
-Aldosterone promotes Na+ and water retention, causing plasma volume expansion, which then shuts off renin secretion
-In the supine state, there is a diurnal rhythm of aldosterone and renin secretion; the highest values are in the early morning before awakening
-angiotensin converting enzyme converts angiotensin 1 to 2
-changes Na, water, fluid levels
-dont really worry about this!
action of aldosterone on principle cell of collecting duct
-modulates Na reabsorption
-feedback mechanism regulating aldosterone secretion
countercurrent multiplier
-Maintains NaCl concentration gradients in medullary interstitial fluid
-Helps conserve water in response to ADH
what conditions would affect glomerular filtration
-HTN- more filtration
-hypotension- less filtration
-RTS- less filtration
-obstruction- less filtration
-hypovolemia- less filtration
-damage to glomerulus- more filtration (leaking)
-adrenal issues
-ADH
-stress- high
-chronic stress- low
bloop pressure/resistance
-two areas of resistance- afferent and efferent arterioles
-constriction at efferent arteriole- increase filtration (more pressure)
-dilate efferent arteriole- decrease filtration
-constrict afferent arteriole- decrease filtration
-dilate afferent arteriole- increase filtration (more flow)
effects of afferent and efferent tone
-RBF- renal blood flow
-case- pt with HTN taking an ACE inhibitor and NSAIDS for chronic knee pain -> acute renal failure (BOARDS AND TEST)
-PGC, glomerular capillary hydrostatic pressure
-FF, filtration fraction
renal blood flow- key points
-20-25% of cardiac output is received by kidneys
-Low vascular resistance permits high flow
-High O2 demand for renal metabolism
-Systemic perfusion pressure of 90-100mmHg needed -> < 90 -> decrease filtration
-Risk of damage in shock, dehydration, ischemic events
kidneys: EPO and vitamin D
-feedback loop
-important in chronic kidney disease
typical tests ordered include
-Metabolic profile (basic or complete)
-BUN (blood urea nitrogen) and creatinine are key players- tells us kidney function
-Blood sample for:
-CBC, culture, special markers of inflammation *(high platelets or low)
-anemia, lack of EPO, WBC
-ESR and CRP
-Urinalysis
-Urine for:
-Spot electrolytes, microscopy (casts), culture
-Imagining tests
-Key imaging test in Nephrology/GU is the Ultrasound (first imaging test)
-Other tests of use are: x-ray, CT with IV contrast, urinary cystogram
-CT w/o contrast- chronic kidney disease, renal insufficiency (toxic) -> dont use on kidney stones -> everything will look white
-cystoscopy
estimated eGFR: Cockroft-Gault formula
-Requires:
-Age
-Gender
-Plasma/serum creatinine
-Weight
-eGFR =
(140-age) x weight / (72 x creatinine)
x 0.85 (if female)
-just know the variables
-as we age -> kidneys get worse
-as we loss lean muscle mass -> kidneys get better -it evens out -> GFR is generally the same throughout life
estimated eGFR: eGFR 2021 CKD EPI creatintine equation
-Laboratory calculated
-No longer utilizes race in its equation
-Prior equation utilized race
estimated eGFR- cystatin C
-Protein whose level is related to renal function
High level corresponds to decreased renal function
-variables dont affect this value -> not used yet
uses of the eGFR
-Medication management
-1/2 the dose if its a renal excreted drug
-Safety during procedures
-Staging of disease
-Chronic Kidney Disease
-Staging
-Planning
diagnostic imaging- x-ray
-A-P (antero-posterior) x-ray image of abdomen and pelvis to evaluate:
-Kidneys
-Ureters
-Bladder
-not used often
diagnostic imaging- renal ultrasound
-Use of ultrasound to image renal and bladder structure
-Use of Doppler can help evaluate renal blood flow
-used often
diagnostic imaging- cystography
-Radiocontrast medium is instilled via urinary catheter
-May be also useful for vesicoureteral reflux evaluation (shown in pic)
-catheter inserted and balloon inflated to prevent it coming out -> contrast injected
-urine is seen flowing retrograde into ureter
-valve is incompetent
-urine flows backward
-chronic UTI
-pyelonephritis!
diagnostic imaging- urinary pyelogram
-IV contrast excreted by kidneys
-X-rays are taken at intervals
-Giving a functional image of the urinary system
-calyx, pelvis lights up
-issues with function
-decrease in contrast in certain areas -> narrowing on the right side
diagnostic imaging- CT with IV contrast
-CT scan using IV contrast used for structural evaluation of kidneys
-renal artery is bumpy -> renal artery stenosis
-string-of-beads sign
risk with IV contrast
-Allergic reactions
-Adverse effect to kidney function
-Extravasation (common)
-Ice pack site
-Painful
-Evaluate for distal flow and necrosis
-ulcer and edema
diagnostic imaging- ureteroscopy
-Endoscopic examination of the upper GU tract
-Endoscope is passed through urethra to bladder
difference between nephrotic and nephritic syndrome
-NEPHROTIC SYNDROME:
-Inc’d protein in urine
-Dec’d protein in serum
-Generalized and facial edema
-Inflammation leads to increased glomerular permeability (due to damage to podocytes)**!!!! -> increase GFR
-Decreased oncotic pressure in the blood
-edema in legs in standing, edema in sacral/coccyx if laying
-NEPHRITIC SYNDROME
-blood in urine
-decreased urine quantity
-hypertension
-destruction of epithelial lining of glomerulus**
-decreased renal perfusion and increased blood pressure
nephrotic syndrome: 24 hours protein urine
-3 – 3.5 gm/24 hour or greater = nephrotic syndrome
-Coupled with serum albumin < 2.5 gm/dL
-facial edema!!!
nephrotic syndrome: primary
-* “Diseases of exlusion – rule out the ‘secondary’ causes first”
-Minimal Change Disease (MCD)
-Focal Segmental Glomerulosclerosis (FSGS)
Membranous glomerulonephritis
-Mesangioal Proliferative Glomerulonephritis (MPGN)
-Rapidly Progressive Glomerulonephritis (RPGN)
nephrotic syndrome: minimal change disease*
-MC cause of nephrotic syndrome in children!!!!!!!!!*
-Normal on light microscopy
-Only histologic causes seen on electron microscope
-bx of glomerulus -> electron microscopy shows loss of podocytes
-on light microscopy its normal!
nephrotic syndrome: focal segmental glomerulosclerosis
-MC cause of nephrotic syndrome in adults
-Tissue scarring seen on microscopy
-Some glomeruli are scarred while others are spared
-some normal, some scar tissue
nephrotic syndrome: Secondary causes
-Diabetic nephropathy*
-Systemic lupus erythematous*
-Sarcoidosis*
-Syphillis
-Hepatitis B/C
-HIV
-Sjogren’s syndrome
-Amyloidosis
-Multiple myeloma
-Other cancers
-Vasculitis
-Medications
-Gold salts, PCN, captopril…
nephrotic syndrome: tx of the actual kidney injury
-tx the underlying cause! and also do this:
-Corticosteroids
-Prednisone
-60mg/m2 daily for 8 weeks
-Then 40mg/m2 for 4 weeks
-Then taper
-~Avg adult dosing is 100-120mg/day to start
-Assess responsiveness to treatment
-Watch for side effects of corticosteroids
-Immunosuppressive agents
-Used if nephrotic syndrome is reoccurring or non-responsive to corticosteroids
-Cyclophosphamide is typically used
nephrotic syndrome: tx by complications
-Correct the underlying cause if secondary cause is present
-Hyperlipidemia
-Diet restriction
-Statins, fibrates
-Hypercoagulability- Low molecular weight heparin
-Edema:
-Correct protein intake with lean protein -> No more than 1gm/kg/day
-Limit water intake to amount lost
-Limit sodium to 1-2gm/day
-Diuretics (Loop diuretics) -> injury is at the glomerulus not the loop! -> its okay!
-Hypoaluminemia
-Dietary protein
nephritic syndrome
-Post-streptococcal glomerulonephritis- from rheumatic fever
-Focal proliferative
-Alport Syndrome
-SLE
-IgA nephropathy
-Chronic hepatic failure
-Celiac sprue
-Diffuse Proliferative
-Membranoproliferative:
-Hepatitis B/C
-SLE
-Sickle cell disease
-> Rapidly progressing glomerulonephritis
Goodpastures syndrome
-Autoimmune disorder affecting both
-Pulmonary
-Renal
-Signs and Symptoms:
-Hemoptysis!
-Hematuria/proteinuria!
-Nephrotic/nephritic symptoms
-Malaise/fever/chills
-Proposed cause:
-Immune system insult leads to development of anti-GBM (glomerular basement membrane) antibodies
-Treatment:
-Plasmapheresis
-Immunosuppressant therapy
-Cyclophosphamide, prednisone, rituximab
-Prognosis:
-Without treatment 100% mortality
-With treatment, 5-year survival ~ 80%
-Epidemiology
-1 per million people per year
-Bimodal age distribution:
-20-30 and 60-70 y/o affected most!
review key points
Understand basics of the renal physiology and anatomy
How does the process of renal filtration occur
Understand several key diagnostic tests and what they can indicate
How will I use them to assess renal function or dysfunction?
Differentiate between nephrotic and nephritic syndrome.
How will the patient with one of these disorders present and what do I do to make the diagnosis?
