Renal Flashcards
Proximal convoluted tubule absorption
- Almost complete absorption of important substances
- Absorption H2O 60%, HCO3 90%, Na, Cl, K, amino acids, glucose, nutrients
- PTH acts to increase PO4 excretion
- 65% glomerular filtrate absorbed, not concentrated
Loop of Henle absorption
- Reabsorbs H2O 30%, Na, Cl
- Concentrates urine
- PTH acts to increase Ca reabsorption
Distal convoluted tubule absorption
- Reabsorbs H2O, HCO3, Na, Cl
- Secretes K, H
- Regulates pH and dilutes urine
- Aldosterone acts on Na channel to resorb H2O and Na to maintain intravascular volume
- Fine tuning electrolytes
Collecting duct absorption
- Derived from ureteric bud
- Final Na, Cl, Urea, J2O reabsorption
- ADH - creates aquaporins that insert in to membrane to allow for water permeability
Renin Angiotensin System
Renin (kidney) -> Angiotensinogen (liver) -> Angiotensin I (lung) -> Angiotensin II (ACE)
- > Aldosterone (adrenal)
- > arteries -> vasoconstriction -> increase BP
- > Na + H2O retention (kidney) -> increase BP
Renin
Aims to increase BP
- Released in response to LOW Na and LOW intravascular volume, LOW BP
- Suppressed by ADH, Angiotensin II, High Na, High K
Aldosterone
Aims to increase BP
- Acts on ENAC Na Channel in distal tubule to resorb H2O + Na to maintain intravascular volume. Secretes K + H
- Stimulated by Angiotensin II, High K, Low Na
- Inhibited by ANP, high Na
Low Aldosterone: LOW BP, LOW Na, High K, acidosis, weight loss e.g. CAH
High Aldosterone: HIGH BP, low K, alkalosis
ADH
- Triggered by: LOW BP, pain, nausea, pregnancy
- Inhibited by: caffeine, alcohol
- Acts on collecting duct - inserts aquaporins to allow for water to be reabsorbed
ANP
- Triggered by HIGH BP in response to arterial stretch
- Dilates afferent, constricts efferent arterioles
- Inhibits aldosterone and renin secretion
- Inhibits ADH action on kidney
- Inhibits NaCl reabsorption in collecting duct
Afferent and efferent arterioles
Afferent arteriole dilation + efferent arteriole constriction = increased GFR
Efferent arteriole constriction + efferent arteriole constriction = reduced GFR
- Afferent Arteriole Dilatation: Low BP, prostaglandin, Dopamine (low dose), ANP, NO
- Efferent Arteriole Constriction: Angiotensin II (low dose)
- Afferent Arteriole Constriction: High BP, exercise, shock, angiotensin II (high dose), noradrenaline, endothelin, ADH
- Efferent Arteriole Dilatation: Angiotensin II blockade
HYPOVOLAEMIA = increased renin, increased aldosterone, increased Na reabsorption
LOW NA = low ANP, high aldosterone, high angiotensin II
Renal tubular acidosis
Consider if normal anion gap metabolic acidosis
AG = Na - (Cl+HCO3), high Cl)
Type 1 - Distal RTA
- Can’t excrete H
- Normal anion gap metabolic acidosis
- Normal Na, LOW K, High urine Ca, urine pH >5.8
- Nephrocalcinosis, bone disease, rickets
- Presents <1yo with FTT, parent has renal stone disease
- Can have SNHL
- Associated with Marfans, Elhers Danlos, Wilsons, VUR
Type 2 - Proximal RTA
- Reduced HCO3 resorption
- Metabolic acidosis
- Low Na, LOW K, LOW PO4, glycosuria, urine pH <5.8
- Polyuria, growth failure, anorexia, vomiting
- Associated with Fanconi syndrome
Type 4 - Collecting duct
- Aldosterone deficiency/insensitivity
- Metabolic acidosis
- Low Na, HIGH K, high H, urine pH <5.8
- e.g. post obstructive diuresis (UTI, obstructive uropathy), CAH
Nephritic syndrome
Haematuria, hypertension, AKI, oliguria, oedema
Nephritic syndrome - low complement
Post Strep GN
- 4-12 yo, 10-14 days post group A beta haemolytic strep, 3-6 weeks post skin infection
- Tea coloured urine, RBC acts, ASOT pos
- Low C3/4 normalises by 6/52 biopsy if persists (think SLE or membranoproliferative if continues
SLE
- ANA pos most, dsDNA pos most
- C3/C4 low - C3 normalises with treatment C3 marker of disease activity
- Biopsy all the IG
- Rx steroids, immunosuppression
Membranoproliferative GN
- C3/C4 persistently low
- Biopsy widened basement membrane due to infiltrates
Shunt nephritis
- Staph aureus
- Fevere, arthralgia, hepatosplenomegaly, lethargy, nephritis
- Low C3/C4
- Rx antibiotics
Nephritis syndrome - normal complement
IgA nephropathy
- At time of throat infection
- Most common cause of macroscopic haematuria
- Associated with autoimmune (SLE, coeliac, IBD)
- IgA can be normal, normal C3
- Biopsy - IgA deposits in glomeulus
- Rx: steroids
Alports
- X linked (mild in females)
- Type IV collagen (glomerular basement membrane(
- Macroscopic haematuria, SNHL, cataracts, anterior lenticonus
- Biopsy - splitting of basement membrane
HSP Anti GBM (Good pastures)
Nephrotic syndrome
Proteinuria, hypoalbuminaemia, oedema
Congenital
- Finnish type** no NPHS1 (nephrin)
- Non-Finnish type no NPHS2 (podicin)
- Asscoiated with Denys Drash
Minimal change**
- Preschool age
- No macroscopic haematuria
- Light microscopy normal, electron micro fused podocyte foot processes
- 20% steroid resistant
Membranoproliferative/mesangiocapillary
- > 10 yo
- Macroscopic haematuria
- Consider if thought to be PSGN but C3 doesn’t resolve
- 20% steroid resistant
Focal Segmental Glomerulosclerosis
- > 6yo
- Tea coloured urine
- RBC casts
- Glycosuria
- Focal sclerotic lesions on biopsy
- IgM C3 positive on stain
- ESRF
- 80% steroid resistant
Membranous nephropathy
- Older children
- Biopsy - thick capillary walls, IgG deposits
Mixed/GN
Rapidly progressive GN
- Rapid decline in renal function
- Heavy proteinuria, hypertension, ongoing low complement
- Crescent cells on biopsy
- Rx: steroids, cyclophosphamide
- ESRF in weeks (end point of many Dx)
Steroid resistance - 10% mutations in NPHS2 (podicin)
Nephronophthisis
Commonest genetic form of renal failure Ciliopathy NPHP genee Growth failure, pale Progress to renal failure Benign urine micro Sodium bicarb Transplant cures
Renal angiomyolipomata
TS
Usually bilateral
Can cause fatal spontaneous bleeding
Grows and encroaches on renal tissue –> ESRF
Fanconi syndrome
Type 2 RTA proximal FTT, polyuria LOW PO4, HCO3, Na, K, amino acids Glycosuria Supplement PO4, HCO3, K, calcitriol
Renal osteodystrophy
HIGH PO4, HIGH PTH
LOW Vit D (1,25OH), LOW Ca
Monitor PTH
Tx: calcium carbonate (PO4 binder), Vit D if PTH stays high
Tubular interstitial nephritis
Drugs (NSAIDS, penicillin), infection
Fever, arthralgia, rash, macroscopic haematuria
Casts in urine
Pulmonary renal syndrome
ANCA associated vasculitis most common
Wegners
Granulomas
cANCA (ear/nose/throat vasculitis, sinusitis, granulomatous lung vasculitis, Staph. Crescenteric pauci immune GN no deposition of Ab)
Microscopic polyangitis pANCA
HSP
Ig A mediated
URTI prior, rash, arthritis, abdominal pain, haematuria, proteinuria, hypertension
Complications - renal, intussusception, CNS vasculitis
Steroids (reduced Sx not complications)
HUS
Typical E coli 0157:h& shigatoxin
Atypical pneumococcal, complement
Haemolytic anemia, thrombocytopaenia, AKI, fragmentation on film
High LDH, low haptoglobin, DAT neg in typical
Bartter syndrome
Autosomal recessive LOH gene Collecting duct - same response as LOOP diuretic - frusemide Polyuria, polydipsia, nephrocalcinosis Metabolic alkalosis LOW Na, LOW K, LOW Cl, HIGH urine Ca Replace salt/IVF
Gitelman syndrome
Autosomal recessive
Same as thiazide diuretic e.g. hydrochlorothiazide
Nocturia, joint pain
LOW K, LOW H, LOW Mg, normal Ca, LOW urine Ca
High serum glucose, high uric acid
Rx: KCL supps
Prune Belly
Abdominal wall defect, undescended testes, infertility, VSD, malrotation
Denys Drash
WT1
Congenital nephrotic syndrome, Wilm’s thymus, sex disorder (hermaphroditism)
Bardel-Beidl
Obesity, hypogonadism, polydactyly, developmental delay, renal cysts
Multi cystic dysplastic
Large peripheral cysts no renal parenchyma (other kidney should hypertrophy if normal)
MAG3 won’t take up tracer
Involut4es then disappears
Long term follow up risk Wilms in remaining kidney
ARPKD
Both kidneys enlarged, multiple cysts in cortex and medulla
Associated hepatic fibrosis/hepatic cysts
Need to check siblings
50% CKD by 20yo
Potter syndrome
Severe version ARPKD significant oligohydramnios - pulmonary hypoplasia, DDH etc
ADPKD
Common
Bilateral enlarged kidneys
>2 cysts
Can have in liver, pancreas, spleen, ovaries
Associated with berry aneurysms
Hypertension monitors disease progr4ession
Stones
Usually have high urine Ca
Fluids
Low salt diet and Potassium citrate protective
Calcium oxalate sontes - most common
Struvite stones - associated with proteus UTI/underlying anatomical problems
Consider if FTT recurrent urosepsis
Uric acid stones - not seen on XR
Renal cysts and diabet4es
AD HNF1B
Renal cysts
MODY
Horseshoe kidney
Associated with VACTERL, trisomy, GDM
Ectopic ureter
Think if constant wetting day and night
Duplex kidney
Risk of obstruction where ureters overlap
PUJ obstruction
Most common
Bilateral 40%
MAG3
Tx: pyeloplasty, antibiotic prophylaxis
VUR reflux
Complications: hypertension, recurrent UTI, reflux nephropathy
Dx: MAG3
Grade 1-3 prophylactic Abs, Grade 4-5
`PUV
Dx MCUG
Tx: valve ablation, vesicostomy, transplant
Testicular torsion
Acute, excruciating, urine NAD
Toersion of the appendix testes
Gradual, tender upper pole blue dot sign
Epidydimo-orchitis
Rare pre puberty
Fever, red, swollen, painful
Bactrim
Adolescents - chlamydia, gonorrhoea
Nocturnal enuresis
5 yo 20%
10yo 5%
Alarm (motivation)
Desmopressin
Urinary incontinence
Day and night
>5yo
Improve voiding habits
Oxybutinin
RBC casts
GN
Tubular epithelial cells/casts
TIN
Granular casts (muddy brown)
ATN
FGF23
Marker for bone disease
High in X linked phosphotaemic rickets
TTKG
Tests the response of distal tubule to aldosterone
MCU
Reflux**
Valves**
Duplex system
DMSA
Function
Scarring**
Function of kidney
MAG3
Function and excretion
PUJ obstruction**
Histology
Exudate (infiltration by neutrophils) P Strep GN
Normal high micros, fused podocytes on EM - Minimal change disease
Crescent cells - rapidly progressive GN**, ANCA associated, anti-GBM, SLE
Fractional excretion
Plasma Cr x Urinary Na /
Urinary Cr x Plasma Na
ARF = <1% prerenal >1% renal >4% post renal
GFR
Urine concentration x
Volume/
Plasma Concentration
Depends on renal blood flow Adult level by 2yo Inulin gold standard (can't measure) 51-Cr EDTA most accurate Cr overestimates GFR (Cr secreted by tubules)
Loop diuretics
E.g. Frusemide
Inhibits Na/K/Cl cotransporter
SE: low K/Na/Cl/Ca/Mg
LOOP = LOW EVERYTHING
Gout, high BSL, high lipids
Thiazide diuretics
E.g. Hydrochlorothiazide
Inhibits resorption of NaCl SE: Low K, Na, Cl High Ca Abnormal BSL, lipids Gout
Potassium sparing diuretics
E.g. spironolactone
Block aldosterone activity in DCT/CD to stop H2O resorption
Uses: with loops or thiazide to help keep K stable
SE: high K, gynaecomastia
Calcineurin inhibitors
Cyclosporin
- Hirsutism, gingival hyperplasia, hyperlipidaemia, hypertension, T2DM
Tacrolimus
- *CYP450, hyperglycaemia, T2DM, low Mg, diarrhoea, seizures
Anti-proliferative drugs
Inhibit nucleotide synthesis
Methotrexate
- BM suppression, hepatic fibrosis, mucositis, interstitial pneumonitis
Mycophenolate
- Severe diarrhoea, leukopenia, pulmonary fibrosis
Azathioprine
- Agranulocytosis, infection, lymphoma 4x risk, hepatotoxicity, pancreatitis
Sirolimus
- Pancytopaenia, mouth ulcers, abnormal LFTs
Alkylating agents
Impair DNA replication
Cyclophosphamide
- Sterility, hemorrhagic cystitis, BM suppression, leukaemia, alopecia
Monoclonal antibodies
TNF inhibitors e.g. infliximab, etanercept
- Heart failure, opportunistic infections, lymphoproliferative disease check TB prior
B cell depletes e.g. rituximab
- Hypersensitivity reactions, flu like illness, enterovirus, meningitis, reactivation of Hep B
Interleukin inhibitors e.g. tocilizumab IL6, anakinra IL2
Other drugs
Cystinuria - penicillamine
Hydroxyurea - pyridoxine
Uric acid stones - allopurinol
Hypercalcuria - thiazide
