Renal Flashcards
What is a normal GFR?
100 mL/min
What is used to estimate RPF?
PAH clearance
What is a normal Na+ and K+ level in the blood?
Na+= 135-145 K+= 3.5-5
What is a normal BUN, Cr, and BUN/ Cr ratio?
BUN= 7-20 Cr= 0.6-1.2 BUN:Cr= 15:1
What is normal CO2, bicarbonate, and pH of the blood?
CO2= about 40 HCO3- = about 24 PH= 7.35-7.45
What is a normal level of albumin in the blood?
3.5-5.5
What does natriuresis mean?
Excretion of Na+ in the urine
What does “oliguria” mean?
Low urine output
Which germ layer do kidneys develop from in embryo?
The mesoderm
What are the 3 names for the stages of the developing kidney?
1) pronephros (degenerates)
2) mesonephros (degenerates)
3) metanephros (becomes adult kidney)
What does the ureteric bud form in embryo?
The collecting system (ureter, pelvises, calyces) and collecting duct
What does the metanephric mesenchyme form in embryo?
All parts of the nephron except the collecting duct (the ureteric bud forms this)
What is unilateral renal angenesis?
You don’t have 1 of your kidneys
The ureteric bud (which forms the collecting system and collecting duct) fails to form—> no signals sent to metanephric mesenchyme for it to differentiate (and form all the parts of the nephron except the CD)—> you get complete abscence of a kidney + ureter
What is multicystic dysplastic kidney?
When the ureteric bud forms, but does not send the signals to stimulate differentiation of the metanephric mesenchyme—> one kidney is unfunctional like a cyst
What is vesicoureteral reflux?
When there is backflow of urine from the bladder up to the kidneys. Results from abnormal insertion of the ureters into the bladder. (Associated with duplex ureters)
What is a duplex collecting system? What conditions is it associated with.
A congenital problem where the baby has 2 ureters on one side (and just 1 like normal on the other side). Due to bifurcation of the ureteric bud (which forms the ureters) before it enters the metanephric blastema.
Strongly associated with vesicoureteral reflux (backflow of urine from ureters up to kidneys) bc if the ureters form abnormally, they often insert abnormally. Also associated with urethral obstruction. Increases risk for UTIs.
Describe Potter syndrome.
Collection of symptoms due to dec amniotic fluid.
Baby has a kidney problem: autosomal recessive Polycystic kidney disease (ARPKD), obstructive uropahty, bilateral renal agenesis (kidneys don’t form on either side), or chronic placental insufficiency—> not peeing—> dec amniotic fluid (oligohydraminos)—> smushed face, limb deformities, pulmonary hypoplasia (underdeveloped lungs bc baby swallows amniotic fluid to expand and further develop lungs) and death.
Mnemonic: “POTTER” Pulmonary hypoplasia, Oligohydramnios (trigger), Twisted face, Twisted skin, Extremity defects, Renal Failure (in utero).
What is posterior urethral valves?
Congenital defect in baby boys. A tissue flap obstructs urine outflow from the bladder—> urine builds up in the kidneys (hydronephrosis).
*this is the most common cause of bladder obstruction in male infants.
A baby boy has a bladder obstruction. What is the most likely cause?
Posterior Urethral Valves.
Congenital defect in baby boys. A tissue flap obstructs urine outflow from the bladder—> urine builds up in the kidneys (hydronephrosis).
*this is the most common cause of bladder obstruction in male infants.
What is “horseshoe kidney?”
When the inferior parts of the 2 kidneys are linked together—> kidneys cannot ascend in the pelvis like they normally do during development so they stay lower in the pelvis (they get stuck below the INFERIOR MESENTERIC ARTERY).
Which congenital abnormality of the kidneys is associated with Turner syndrome?
Horseshoe kidney
What is the urachus?
Embryolical structure that connects the dome of the bladder to the umbilicus. This is obliterated at birth—> median umbilical ligament.
An adult has painless hematuria (common sign of bladder CA) and cancer is found at dome of bladder. Pathology shows it is adenocarcinoma. Where did this come from?
The embryological structure: the urachus.
Urachal remnants can lead to adenocarcinoma of the bladder
If the urachus fails to obliterate at birth, what will be seen?
Urine leaking from the belly button (bc the urachus connects the dome of the bladder to the umbilicus…normally goes away before birth and becomes the median umbilical ligament).
What is hydronephrosis?
Increased fluid in the kidney from back up (for example, if there is bladder obstruction and urine cannot get out to go down through ureters, the urine will stay behind in the kidneys)
What’s the difference between central and nephrogenic diabetes insipidous?
Central DI- not producing ADH
Nephrogenic DI- not responding to ADH
Which types of kidney stones are more likely to precipitate/ form with acidic pH urine? What about with alkaline urine?
Precipitates with low pH (acidic) urine—> Uric acid stones AND cystine stones
Precipitates with high pH (alkaline) urine—> Calcium phosphate stones AND ammonium magnesium phosphate (struvite) stones
What is tumor lysis syndrome and how does it relate to kidney stone formation?
Tumor lysis syndrome= complication of chemo where a bunch of cells are killed at the same time and release their contents like K+, phosphorous, and uric acid into the bloodstream.
This will increase risk for development of kidney stones (for example, uric acid stone—so hydrate and alkalize urine to prevent this type).
Which segments of the nephron have the lowest pH (most acidic/ most H+)?
The DCT and CD
What are the 4 CAUSES of the Potter sequence?
Autosomal recessive polycystic kidney disease (ARPKD), obstructive uropathy (ex: posterior urethral valves), bilateral renal agenesis, chronic placental insufficiency
What affect will a beta-blocker have on renin, ATI, ATII, Aldosterone, and Bradykinin?
A beta-blocker will DECREASE renin, ATI, ATII, Aldosterone (because it inhibits renin, and everything else is downstream from that) and will NOT CHANGE bradykinin levels (only ACE is involved with bradykinin breakdown).
Why can a beta-blocker be used to treat hypertension?
The beta-1 receptor on the kidneys increases renin release. This is one of the receptors a beta-blocker will inhibit—> decreased renin release—> dec ATI—> dec ATII—> dec Aldosterone (dec Na+ reabsorption)—> dec BP.
What is the inheritance pattern of cystic fibrosis (CF)?
Autosomal recessive.
Explain altitude sickness. What drug can help it and why?
High altitude (hypoxia= dec oxygen)—> hyperventilation (blow off more CO2)—> dec CO2= metabolic alkalosis. Kidneys will compensate by dec bicarbonate reabsorption and H+ secretion (we want less bicarb in the blood and more H+ to stay in blood to compensate with a metabolic acidosis over days). RBCs will also increase their molecule 2,3-BPG, which stimulates Hb to unload oxygen and deliver it to tissues. Acetazolamide (Carbonic Anhydrase Inhibitor) can help the body compensate faster (and thus reduce altitude sickness symptoms) by dec bicarb reabsorption.
What’s the difference between central and nephrogenic diabetes insipidous (DI)?
Central DI- you’re not making ADH
Nephrogenic DI- you’re not responding to ADH
(Pee more: body is more concentrated, urine is more dilute)
What is the equation to estimate RPF (renal plasma flow)? What is the equation to calculate RBF (renal blood flow)?
RPF can be estimated by the clearance of PAH.
RPF= Cl of PAH= ([PAH]in urine * V)/ [PAH]in blood, where V= urine volume flow rate
RBF= RPF/ (1-hematocrit)
What triad of symptoms may be seen in Renal Cell Carcinoma (RCC)? Pathogenesis involves loss of what tumor suppressor gene?
Hematuria (peeing out blood), palpable mass, and flank pain (*though often all 3 aren’t seen together).
Loss of VHL (3p) tumor suppressor gene
Drugs that end in “-sartan” are what kind of drugs?
ARBs (angiotensin II receptor blockers)
You have a patient on a beta-blocker to manage his/her HTN. They hate it because they are coughing a lot. What medication can you switch them to?
an ARB (angiotensin II receptor blocker) *ARBs do the same thing as ACE inhibitors (block the RAAS from elevating BP, etc.) but don’t come along with cough and angioedema as side effects since not involved with Bradykinin. ARBs just aren’t quite as good, so we usually prescribe an ACE inhibitor first.
What is hydronephrosis?
Dilation of renal pelvis and calyces. Usually caused by urinary tract obstruction (ex: renal stones, severe BPH, cervical CA, injury to ureter). Other causes include retroperitoneal fibrosis, vesicoureteral reflux.
You’re in metabolic acidosis. How will the lungs immediately compensate? What will the kidneys try to do (3 things) to try to compensate?
Metabolic acidosis= low bicarb.
The lungs will dec CO2 (hyperventilate) to compensate.
The kidneys will: (1) reabsorb more bicarb in the PCT (you have low bicarb so you need to push more into the blood to increase it back to normal), (2) increases H+ secretion throughout the nephron (you have acidosis so you want to pee out more acid), (3) makes more buffer (HPO4(2-) and NH3) so that H+ can be secreted w/o changing the pH of the urine by too much.
What is the detrusor muscle?
Muscle that forms the wall of the bladder. (It is the bladder muscle NOT the pelvic floor muscle)
What is nephrotic syndrome? Explain generally what the problem is and key findings.
Damage to podocytes (from primary cause meaning direct sclerosis or from secondary cause like DM)—> disruption of glomerular charge barrier—> proteins can get through (they shouldn’t be able to)—> pee out a lot of protein (>3.5 g/day)—> less protein left behind in blood (hypoalbuminemia)—> edema (due to less oncotic pressure) and hyperlipidemia (lost protein in blood= thin blood so liver throws excess fat into it to “bulk it up”).
You also see “frothy urine” (from the protein) with fatty casts.
Nephrotic syndrome can cause hypercoagulation due to antithrombin (AT) III lost in urine (AT is a protein that stops coagulation, so if you pee it out—> too much clotting) and inc risk of infection due to loss of immunoglobulins in urine.
