RENAL Flashcards
What are the embryologic sources of renal system?
Pro nephrons degenerates 4 week
Mesonephros male genital contribution
Metanephros uerteric bud until collector tubes // metanephric mesenchyme (mesoderm) until distal convoluted tubule
What’s POTTER sequence ?
Pulmonary hypoplasia Oligohydramnios (trigger) Twisted face Twisted skin Extremity defects Renal failure (in utero)
Genetic defects related whit Horseshoe kidney ?
ANEUPLOID DEFECTS
down, Edwards, Patau, turner…
What’s the clearance Ecuation?
Cx = UxV/Px
Cx GFR: net tubular secretion of X.
Cx = GFR: no net secretion or reabsorption.
What’s the GFR Ecuation?
GFR = Uinulin × V/Pinulin
What are the effective renal plasma flow And renal blood flow?
eRPF = UPAH × V/PPAH = CPAH.
RBF = RPF/(1 − Hct).
What’s filtration fraction and filtered load?
Filtration fraction (FF) = GFR/RPF. Normal FF = 20%.
Filtered load (mg/min) = GFR (mL/min)× plasma concentration (mg/mL).
Actions of NSAIDs and ACE inhibitors in bowman capsule
NSAIDs ⬇️GFR ⬇️RPF ↔️FF (afferent 🚫)
ACE inhibitors ⬇️GFR ⬆️RPF ⬇️FF (efferent ✅)
Calculation of reabsorption and secretion rate(4)
Filtered load = GFR × Px.
Excretion rate = V × Ux.
Reabsorption = filtered – excreted.
Secretion = excreted – filtered.
How is the glucose clearance?
∼ 200 mg/dL, glucosuria begins (threshold)
∼ 375 mg/dL, all transporters are fully saturated (Tm).
What’s Hartnup disease?
neutral aminoaciduria and absorption from the gut tryptophan for conversion to niacin pellagra-like symptoms.
Treat with high-protein diet and nicotinic acid.
Which drugs acts in the 4 diferents nephrons segments?
EARLY PCT
ACE inhibitors 🚫Na/H exchange
ACETAZOLAMIDE 🚫carbonic anidrase
THICK ASCENDING LOOP
Loop diuretics 🚫NA,K,Cl co-transporter
EARLY DCT
Thiazides diuretics 🚫NA,Cl co transporter
⬆️Ca/Na exchanger PTH
COLLECTING TUBULE
Amiloride triamterene 🚫 Na channels
Espironolactone 🚫aldosterone receptores
Whats the fundación of ALDOSTERONE in Collecting Tubule? (1,3. 2,2.)
✅ In principal cells:⬆️ apical K+ conductance, ⬆️Na+/K+ pump, ⬆️ENaC channels ⏩lumen negativity ⏩K+ loss.
✅In α-intercalated cells: ⬆️ H+ ATPase activity⏩⬆️ HCO3−/Cl− exchanger activity.
Whats the función of ADH in Collecting tubule?
✅ADH—acts at V2 receptor⏩ insertion of aquaporin H2O channels on apical side.
Explain renal tubular defects (FaBio Guarnizo Loca)
FANCONI 🚫PCT ⬆️excretion a.a. , glucose, HCO3–, and PO43– metabolic acidosis
BARTTER Affects Na+/K+/2Cl– cotransporter.metabolic alkalosis ⬆️U Ca
GITELMAN Affects NaCl reabsortion DCT Hypokalemia , hypomagnesemia, hypocalsuria ,metabolic alkalosis.
LIDDLE ⬆️Na reabsortion ⬆️TA hypokalemia metabolic alkalosis ⬇️aldosterone tto Amiloride
What’s Syndrome of apparent mineralocorticoid excess?
Hereditary deficiency of 11β-hydroxysteroid dehydrogenase
TOO MUCCH CORTISOL
⬆️mineralocorticoid activity
⬆️TA,hypokalemia,metabolic alkalosis.
What’s the action of ANP BNP?
relaxes vascular smooth muscle via cGMP⏩ ⬆️GFR ⬇️renin
⬆️Na+ filtration with no compensatory Na+ reabsorption
What’s the function of juxtaglomerular aparatus?
JG cells secret RENIN ( B1 receptors ⏩renin) BBs⏩ ⬇️renin
MACULA DENSA sense ⬇️NaCl ⏩adenosine⏩vasoconstriction
Action of PTH to ⬆️ Ca reabsortion
✅1α-hydroxylase
Convert 25-OH D3⏩1,25-(OH)2 D3
Action of ATII
Efferent constriction ⏩⬆️GFR and ⬆️FF but with compensatory Na+ reabsorption
Which situations cause hyperkalemia? DO LAβS.
Digitalis (blocks Na+/K+ ATPase)
HyperOsmolarity
Lysis of cells (e.g., crush injury, rhabdomyolysis, cancer)
Acidosis
β-blocker ⬇️Na+/K+ ATPase
High blood Sugar (insulin deficiency)
What’s the predicted PCO2 from Metabolic Acidosis
Pco2 =1.5[HCO3–]+8±2
Types of renal tubular acidosis (3)
Distal (type 1), urine pH > 5.5 Hypokalemia ⬇️H secretion
Proximal (type 2), urine pH
Ethology of urine Casts (6)
RBC casts glomerulonephritis malignant hypertension
WBC casts acute pyelonephritis transplant resection
Fatty casts (“oval fat bodies”) Nephrotic Syndrome
Granular (“muddy brown”) Acute Tubular Necrosis
Waxy casts CRF
Hyaline casts Non specific
What are the Nephritic syndromes (5)
Which is a GBM Damage
- Acute poststreptococcal glomerulonephritis
- Rapidly progressive glomerulonephritis
• IgA nephropathy (Berger disease)
• Alport syndrome
• Membranoproliferative glomerulonephritis
What are the Nephrotic Syndromes (5)?
Which is Podocyte Disruption
- Focal segmental glomerulosclerosis (1° or 2°)
- Minimal change disease (1° or 2°)
• Membranous nephropathy (1° or 2°)
• Amyloidosis (2°)
• Diabetic glomerulonephropathy (2°)
What are the Nephritic - Nephrotic Syndromes(2)
Which is a severe GBM damage
• Diffuse proliferative glomerulonephritis
• Membranoproliferative glomerulonephritis
Lab findings in Acute poststreptococcal glomerulonephritis(4)
Cola-colored urine
IF—(“starry sky”) granular appearance (“lumpy-bumpy”)
⬆️ anti-DNase B titers
⬇️complement levels
Microscopic findings in Rapidly progressive (crescentic) glomerulonephritis (RPGN) and cells , type of hypersensitivity
LM and IF—crescent moon shape
glomerular parietal cells, monocytes, macrophages.
Type II hypersensitivity
What diseases can provoke RPGN (3)
Goodpasture syndrome—type II linear IF HEMATURIA/HEMOPTYSIS
IMMUNE -COMPLEX : postestreptococal , SLE, Ig A, Henoch-shonlein
Granulomatosis with polyangiitis (Wegener) PR3-ANCA/c-ANCA. Microscopic polyangiitis MPO-ANCA/p-ANCA.
How is seen in LM and IF the Diffuse proliferative glomerulonephritis (DPGN)
Due to LES
LM—“wire looping”
IF—granular
How is seen Ig A nephropaty (Berger Disease)
IF—IgA-based IC deposits in mesangium proliferation
How is seen Alport Syndrome?
Mutation type IV collagen
thinning and splitting of glomerular basement membrane
can’t see, can’t pee, can’t hear
How is seen Membrano proliferative glomerulonephritis (MPGN)
Type I—subendothelial immune complex “tram-track” GBM splitting caused by mesangial ingrowth.
Type II—intramembranous IC deposits; “dense deposits.”
Why in Nephrotic syndrome there is an hypercuagulative and immunodeficiency state?
Antithrombin (AT) III loss in urine
loss of immunoglobulins in urine
Principal features of Focal segmental glomerulosclerosis (2)
EM—effacement of foot process like minimal change disease.
Collapsing glomerulopathy
Proliferation and hypertrophy of epithelial cells
MCC of nephrotic syndrome in African Americans and Hispanics.
Principal features of Minimal change disease (lipoid nephrosis)
EM—effacement (fusion) of foot processes
MCC of nephrotic syndrome in children
GOOD RESPONSE TO ABs
What’s the principal features of Membranus Nephropaty?
EM—“spike and dome” appearance with subepithelial deposits.
MCC of 1° nephrotic syndrome in Caucasian adults.
How is seen Amyloidosis?
LM—Congo red stain shows apple-green birefringence under polarized light.
How is the GFR and permeability in Diabetic Glomerulonephropaty?
GMB thickening
⬆️ Permeability
⬆️ GFR
How is seen calcium stones?
⬆️pH calcium Phosphate
⬇️pH calcium oxalate
RADIOPAQUE!!!!
Hypercalciuria
Normocalcemia
TTO hydratation, tyazides, citrate
Cause of Ammonium, magnesium, phosphate stones
⬆️pH
infection with urease ⊕ bugs (e.g., Proteus mirabilis, Staphylococcus saprophyticus, Klebsiella)
What are the RADIOLUCENT stones?(2)
Utica acid
Cystine Cistinuria Children Sodium cyanide nitroprusside test ⊕
What are the most common renal cancers in children and adults?
ADULTS Renal cell carcinoma from PCT cells
CHILDREN Wilms tumor (nephroblastoma) from embryonic glomerular
What are the associations for transitional cell carcinoma? Pee SAC
Phenacetin
Smoking
Aniline dyes
Cyclophosphamide
Risk factors of Squamous cell carcinoma of the bladder (4)
Schistosoma haematobium infection (Middle East)
chronic cystitis
smoking
chronic nephrolithiasis
What is the characteristic microscopic change of chronic Pyelonephritis?
thyroidization of kidney
Disease related whit diffuse cortical necrosis (2)
Obstetric catastrophes
Septic shock
Keys findings in Acute Tubular Necrosis
⬆️FENa>1
Granular “muddy brown” casts
Stages of Acute tubular necrosis and its etiology
- Inciting event
- Maintenance phase—oliguric; lasts 1–3 weeks; risk of hyperkalemia, metabolic acidosis, uremia
- Recovery phase risk of Hypokalemia
ISCHEMIC
NEPHROTOXIC
What’s Renal Osteodystrophy?
Failure of vitamin D hydroxylation, hypocalcemia, and hyperphosphatemia 2° hyperparathyroidism.
Contraindications of use of mannitol
Anuria
Heart Failure
What are Loop diuretics?(4)
Furosemide
Bumetanide
Torsemide
Ethacrynic acid
What are the toxicity symptoms of Loop diuretics OH DANG!
Ototoxicity, Hypokalemia, Dehydration, Allergy (sulfa), Nephritis (interstitial), Gout.
What are the toxicity symptoms of Thiazides diuretics?(4)
⬆️ Glycemic
⬆️ Lipidemia
⬆️ Uricemia
⬆️ Calcemia
How can identify diuretics by urine labs ? (5)
⬇️ Na : Osmotic ⬇️ K : potassium sparing ⬆️ HCO3 : carbonic anhydrise inhibitor ⬆️ Ca : loop diuretic ⬇️ Ca : thiazide
What are potassium sparing diuretics? (3)
Spironolactone
Eplerenone
Triamterene
Amiloride
What diuretics cause acidemia? (2)
Carbonic anhydrise inhibitors
K sparing
What diuretics cause alkalemia?
Loop diuretics
Thiazides
What are the toxicity symptoms of ACE inhibitors? CATCHH
Cough Angioedema Teratogen ⬆️Creatinine ( ⬇️GFR) Hyperkalemia Hypotension.
Mechanism of action of Aliskiren
Direct renin inhibitor
How is seen in LM biopsy of kidney in HTA and chronic Diabetes?
Homogenous deposition of eosinophilic (pink) hyalin material in the intima and media of small arteries and arterioles HYALINE ATHEROSCLEROSIS
In the embryonic stage what is the structure which communicates the yolk sac and urogenital sinus?
ALLANTOIS!!!!!!
What are the congenital situations in allantois problems?
PATENT URACHUS complete failure of obliteration
URACHAL SINUS failure of close distal
URACHAL CYST failure of central obliteration
What’s the most common pathologic cause of unilateral fetal hydro nephrosis ?
Narrowing of ureteropelvic junction
What’s the most common cause of bilateral fetal hydro nephrosis in boys?
Posterior urethral valves
Which substance is needed to calculate GFR (2)
INULINE or CREATININE!!!!!!!!
Which elements are seen in Fluorescent microscopy in RPGN?
Linear IgG a and C3
Clinical symptoms of goodpasteur, reumatic heart disease, granulomatosis and polyangiitis.
goodpasteur HEMOMPTISIS OLIGURIA
reumatic heart disease JOINT PAIN AND CARDIAC MURMUR
granulomatosis and polyangiitis. NASAL ULCER HEMATURIA
What’s the most important feature to develop in Order to start a Pielonephritis?
Anatomic or Functional Vescicoureteral Reflux
Does the the testicular vessels enter the true pelvis?
NO!!!!!
What’s selective proteinuria?
Albumin loss with minimal loss of the more bulky proteins ( IgG macroglobulin)
What components are most selective in Glomerulus ?
Diaphragms between foot process
GBM
What happen is there is too much acyclovir in the system?
Acyclovir can undergo on crystallization, crystaluria , renal tubular damage in the collecting duct.
What is the effect of lithium in the nephron?
Nephrogenic diabetes insipidus
Antagonist of ADH
How mucho is the mínimum Urine production by a healthy kidney ?
500 ml
What are kimmelsteil-Wilson nodules?
Diagnosis for nodular glomerulosclerosis in diabetic nephropathy
Whit glomerular basement thickening and increased mesangial matrix deposition
What’s the normal anion GAP and how is calculated?
8-12
Anion GAP = Na-[Cl + HCO3]
Differentiate METABOLIC ACIDOSIS
What diseases are related whit focal segmental glomerulonephritis ?(3)
HIV
Heroin abuse
Severe obesity
What type situations are related whit membranous glomerulonephritis ?(4)
TUMORS Solid tumors lung Breast Prostate Colon
SISTEMIC DISEASES SLE DM2
INFECTIONS hepatitis B. C malaria syphilis
DRUGS Gold penicilamine NSAIDs
What type of bacteria is linked whit staghorn stone? (2)
Proteus
Urease ➕
What are staphylococcal antibodies?
Anti DNAasa B
Anti hialuronidase
ASO
How is PSGN IF and EM seen?
IF. Granular deposits of. Ig G, Ig M and C3 in GMB mesangium
EM Subepithelial Humps
What type of of deposits are characteristic in type 1 glomerulonephritis ?
Sub endothelial C1q
What type of deposits are found in LES whit poor prognosis?
Ig E deposits
What blood and serum findings are common in renal cell carcinoma?
⬆️ EPO ( eritrocytosis )
⬆️ PTH ( hypercalcemia )
Histologic characteristics of goodpasteur syndrome?
IF linear deposits
LM crescent formation
How is seen membranoproliferative glomerulosclerosis ?
LM basement membrane splitting
Lobular aparence whit proliferative messangial cells
What is found in focal segmental glomerulosclerosis ?
Ig M
C3
Side effects of somatic diuretic therapy (3)
Dilutional Hyponatremy
Metabolic acidosis
Hypercalemia
What are the causes of stress ,urge and overflow incontinence ?
Stress🔹urethral sphincter disfunction (cough, laugh )
Urge 🔹detrusor overactivity
Overflow🔹 impair detrusor contractility , obstruction
What type of renal cells suffer hyperplasia after arterial renal stenosis?
Yuxtaglomerular apparatus
What nephron son is impermeable to water?
Ascending loop
early distal consulate tubule
Effect of the ADH on the urea?
Increase the Urea absorption in the collecting tubules
What structure has to be transpassing in suprapubic cystostomy?
Anterior abdominal aponeurosis
How tiazides cause Hypokalemia? If tiazides block Na/Cl cotransporters in PCT ?
Leads to hypovolemia activating renine-angiotensin- aldosterone
Enhancing Na/K antiporter
What’s chlortalidone?
TIAZIDE!!!
What a.a. Are not absorbed in cystinuria? COLA
COLA Cysteine Ornithine Lysine Arginine
Difference between metabolic alkalosis saline responsive and saline un-responsive?
Saline Responsibe vomit,nasogastric suction, thiazide/loop diuretic
Saline Un-Responsibe HYPERALDOSTERONISM
Which electrolyte messured in urine is important to evaluate cause of metabolic alkalosis?
CHLORIDE IN URINE
What kind of pathological bladder have patients whit SCLEROSIS MULTIPLE?
Spastic bladder (hypertrophic) Urge incontinence
Where originates the clear cell carcinoma?
PROXIMAL TUBULAR EPITHELIAL CELLS!!!!
Where the quantity of potassium is change. In Hyperkalemic or hypokalemic states ?
COLLECTING DUCT!!!
In the others remain the same
Where is the hight osmolarity?
In the junction of the descending and ascending limbs of Henle
Which substance increase the absorption of urea in collecting duct ( which normally is impermeable to urea)?
ADH!!!!
Which type of cells proliferate and which substance is in the capsule bowman space in RPGN?
PARIETAL CELLS macrophages fiblobalsts
FIBRIN
Drug used in ganciclovir-resistant CMV, and can cause hypocalcemia and hypomagnesemia ?
FOSCARNET!!!!!
⬆️risk of SEIZURES!!!
Features in digital rectal examination in prostate cancer?
Nodules or asymmetric induration
How much increase of serum creatinine is normal (tolerable) after beginning ACE inhibitors?
Up to 30%
Which agents can cause tubular necrosis? (5)
Aminoglycosides Radiocontrast media Cisplatin Amphotericin B Foscarnet
Common drug which cause interstitial nephritis?
METHICILLIN!!!
What is Nesetitide?
BNP analog
How are the coagulation studies in thrombocytopenic thrombotic purpura and hemolytic uremic syndrome?
BT ⬆️
aPTT↔️
PT↔️
What means livedo Reticularis?
Micro-embolism
Effect in the kidney whit chronic use of NSAIDs ? (2)
And what serum cell is elevated?
Chronic interstitial nephritis
Ischemic papillary necrosis
HIGH SERUM EOSINOPHILIC COUNT !!!!!
What’s oxybutinin?
Anti Muscharinic agent used in urge in continence
What nephrogenic disease is related whit palpable purpura?
Henoch-Schonlein purpura. Ig A immune complex
Specific urine finding in minimal change disease in the nephrotic syndrome and what is its cause?
Selective loss of ALBUMIN!!!!
Direct damage of podocytes by IL-13!!!!
What is the WHO classification for renal disease of lupus?
Class I. Normal
Class II mesangial lupus nephritis
Class III focal proliferative glomerulonephritis
Class IV. Diffuse proliferative glomerulonephritis
Class V. Membranous glomerulonephritis
Which arteries supply blood to the ureter?
Renal artery PROXIMAL!!!!!
superior Vesical artery DISTAL!!!!
What type of patient suffers of fibromuscular dysplasia of the renal artery?
Women 20-30 years “strings and beads”
What’s the most common cause of glomerulonephritis?
Ig A nephropaty (Berger disease)
5 DAYS AFTER FLULIKE SYMPTOMS
+ extrarenal symptoms ( abdominal paín, Arthralgias ,purpurik skin lesion) is call HONOCH- SCHONLEIN purpura
How is seen the renal biopsy in Alport syndrome?
Lamellated basement membrane
Whit irregular thinning and thickening
Which a.a. Generates CHO3 in the kidney in acidemia?
Glutamine ⏩ glutamate ⏩ ammonium ➕ HCO3
What are the micturition centers?(3)
SACRAL parasympathetic bladder contraction S2-S4
PONTINE RETICULAR FORMATION relaxation external urethral sphincter
CEREBRAL CORTEX 🚫inhibits sacral
Where the acute tubular necrosis ocurrs?
PROXIMAL TUBULES!!!!!
When renal papillary necrosis ocurrs?(3)
Urinary obstruction /infection Interstitial nephritis (NSAIDs) Microvascular disease
What are the acid buffers used in the collecting duct to enhance the H+ excretion? (2)
HPO4 orthophosphoric acid➡️H2PO4 phosphoric acid
NH3 ammoniac ➡️ NH4 ammonium
Which renal cell carcinoma is associated whit VHL?
Von hippel-Lindau disease chromosome 3q
Renal cell carcinoma
What kind of crystals have pseudogout?
Rhomboidal
CALCIUM PYROPHOSPHATE !!!
Blue parallel
Yellow perpendicular
Antigen implicated with membranous nephropathy ?
Phospholipase A2 receptor
What are the histological findings in acute tubular necrosis?
Proximal tubular cell ballooning and vacuolar degeneration
The finding of oxalate crystals are related whit what kind of poisoning?
Ethylene glycol poisoning
In hepatorenal syndrome how is the renal flow?
RENAL VASOCONSTRICTION!!!!
What is RASBURICASE?
Recombinant version of ureteres oxidase
Take Uric acid and transform to ALLANTOIN (10 times more soluble in urine)
Used in tumor Lysis Syndrome
Important clinical presentation in acute interstitial nephritis by beta-lactamics?(3)
Fever
Rash
Acute renal failure
⬆️eosinophils
⬆️IgE
Drugs which cause tubular vacuolization?
CALCINEURIN INHIBITORS
Tacrolimus
Cyclosporine
Why patients with membranous nephropathy are on risk of thrombotic situations?
URINARY LOSS OF ANTITHROMBIN III !!!!
What’s nutcracker effect ?
Left varicocele by compression of left renal vein by superior mesenteric artery.
How ADH increase the osmotic concentration at the medullary interstisium?
increasing the absortion of Urea at the medullary segment of the collecting tube
What are the High anion gap metabolic acidosis? CATMUDPILES
Normal 10-14
Carbon monoxide/cyanide Alcohol Toluene Methanol Uremia Diabetic ketoacidosis Propylene glycol/ Paraldehyde Isoniazid/Iron Lactic acidosis Ethylene glycol (antifreeze) Salicylates