Renal Flashcards

Question

RTA -focus on management

Answer 1

Membranous Nephropathy (membranous GN) - low sensitivity - higher specificity

Answer 2

Sterile pyuria

Answer 3

Hypoalbuminaemia

Answer 4

**_Salt restriction_**

Answer 5

_**B2 microglobulin Carpal tunnel**_ Dialysis-related amyloidosis is due to deposition of fibrils derived from beta-2 microglobulin, which accumulate in patients with end-stage kidney disease who are being maintained for prolonged periods of time by dialysis. Patients with dialysis-related amyloidosis most commonly complain of shoulder pain related to scapulohumeral periarthritis and rotator cuff infiltration by amyloid, and of symptoms of carpal tunnel syndrome

Answer 6

Change in efferent arteriolar tone Up to 30% is to be expected and does not require medication cessation May actually predict those who are likely to respond

Answer 7

**IgA nephropathy!!!!!**

Answer 8

Cardiovascular disease

Answer 9

Fanconi syndrome — Generalized proximal tubular dysfunction, referred to as Fanconi syndrome, is characterized by **phosphaturia, renal glucosuria (glucosuria with a normal plasma glucose concentration), aminoaciduria, tubular proteinuria, and proximal RTA.**

Answer 10

* **Early (1^st year)** * **Cardiovascular (36%)** * Infection (27%) * Cancer (3%) * **Late (beyond 1^st year)** * **Cancer (30%)** * Cardiovascular (23%) * Infection (12%)

Answer 11

**_Early (1^st year)_** * Graft thrombosis/ technical (38%) * Rejection (24%) * GN (4%) **_Late (beyond 1^st year)_** * “Chronic allograft nephropathy” (CAN) (72%) * GN (7%) * Acute rejection (4%) & Non-adherence (4%) –overlap with CAN? (based on reporting)

Answer 12

CNI = calcineurin inhibitor

Answer 13

(tacrolimus, cyclosporin) * *Isometric vacuolation** of tubular epithelial cells * *Striped** interstitial fibroiss * *Nodular arteriolar hyalinosis**

Answer 14

Humanised **anti-C5 monoclonal antibody** Improves: **Platelet count** (statisically significant), **eGFR** and **quality of life**

Answer 15

Slows progression of CKD Prevention of Bone Buffering Improved nutritional status

Answer 16

sirolimus and everolimus

Answer 17

**_Tubulitis_** (inflammatory cells in the tubualr wall) However, it may occur in other renal diseases as well, e.g., glomerulonephritis and acute tubular necrosis

Answer 18

NO evidence that correcting Ca and PO4 levels BUT no evidence that correcting this imbalnce corrects the risk of mortality - velphoro (sucroferric oxyhydroxide) - PBS approved, expensive, cant be on other non-Ca PO4 binders, not as constipatign very minimal to no absorption of Fe - Calcitriol (ifPTH \> 45) Cinacalcet * Calcium mimetic (next step after phosphate binders)

Answer 19

It's **Galactose-deficient IgA1**

Answer 20

Requiring **dialysis during the first week after transplantation**

Answer 21

Raised **_FGF23_**

Answer 22

i.e before they become oliguric/anuric

Answer 23

**Acute tubular necrosis** ATN, ATN, ATN!

Answer 24

Proteinuria!

Answer 25

Collecting Duct

Answer 26

* urinary eosinophilia * livedo reticularis * vascular risk factors * old males * statins * "blue toe syndrome"

Answer 27

1. Mesangial expansion 2. Glomerular basement membrane thickening 3. Podocyte injury 4. Glomerular sclerosis

Answer 28

Liver cysts in \>80%

Answer 29

* **progression of pre-renal causes** * **ischaemia** for a period of time that leads to **tubular cell death** * Toxins * drugs (vancomycin/gentamicin/amphoteracin) * IV contrast (CT scans/angiography) * Myeloma/immunoglobulins/paraproteins

Answer 30

Bloods * UEC * ANA/ENA/dsDNA/c3 and c4/ANCA (MPO/Pr3)/anti-GBM Ab * ASOT/anti-DNase B * sPEP/serum free light chains Urine * Urine MCS * bland urine sediment * no glomerular red cells, favours pre-renal /ATN/myeloma/interstitial renal disease * active urine sediment - glomerular red cells * seen in acute GN * hyaline/granular/tubular/epithelial casts * suggestive of ATN * Pr/Cr * proteinuria \>1g/day suggestive of glomerula/intrinsic renal disease * uBJP - immunoglobinopathy

Answer 31

* AKI is associated with **adverse outcomes** * AKI associated with increased **mortality**, even when adjusted for comorbidities and severity of illness * Severe AKI requiring RRT in ICU patients is risk factor for death * However the association with mortality is present even for small changes in serum creatinine * Pooled mortality rate for adults with **AKI is 23.9%** * Mortality rate increased with AKI stage CKD following AKI * Some patients with severe AKI do not recover kidney function and remain dialysis dependent * Rate of dialysis dependence at hospital discharge 13-29% * Risk of de novo CKD following reversible, hospital associated AKI in patients with normal pre-hospital kidney function

Answer 32

* *Levels in urine and blood are predictive of pathology** * *_- timely_** detection and reduction in immunosuppression reduces graft loss from 90% to 10-30% - which specific agent is reduced depends on the clinical scenario * *BK DNA in blood t**ends to be used (vriaemia = 50% PPV for BK nephropathy) - **_urine is very sensitive_** so has a **high false positive rate** with regard to infection causing pathology

Answer 33

All virus associated malignancies increased - EBV/HHV-8 - HPV in women causing cervical/vulvar carcinomas Skin - 40% of malignancies in organ transplant recipients, ~50% of those in whites - SCC and BCC account for \>90%. SCC much more common - 2.7x risk of melanoma (highest in renal), and increased mortality associated SCC - low risk = small, well differentiated, low risk site = excise and assess margins - high risk = large, poorly differentiated, high risk site = intraoperative frozen section to ensure margins - Counsel about sun protection and warning signs of malignancy - Regular skin checks dictated by history Solid organ malignancy HR ~2x Haematological malignancy HR ~7x Note that hormone associated malignancy rates aren't increased in transplant patients - breast and prostate cancer specifically

Answer 34

**Calcineurin inhibitors (AEs are all increases)** * Cyclosporine and tacrolimus * **Nephrotoxicity** most common and dose dependent * Hypertension, hyperlipidaemia, hyperkalaemia, tremor, hirsutism (tac causes alopecia), glucose intolerance, **gingival hyperplasia** (tac less everything except more hyperglycaemia) * **Tacrolimus 10-100x more potent** with more predictable oral absorption. Cleared b**y CYPIIIA** so need to watch for inducers and inhibitors * Both associated with increased risk of l**ymphoproliferative malignancies (like azathioprine)** **Mycophenolate** * Non-nucleotide purine metabolism inhibitor * Superior to azathioprine in preventing rejection after renal transplant. Also adopted in liver transplant * **Bone marrow suppression and GI the most common**

Answer 35

* *Prostaglandins and bradykinin** appear to play an important role in dampening the renal vasoconstrictor effects of the sympathetic nerves or angiotensin II - Especially their efferent arteriolar constriction In stressful conditions they **help prevent excessive reduction in GFR** and renal flow - NSAIDs inhibit prostaglandins and so can cause **significant reductions in GFR in such circumstances**

Answer 36

**Amino acids** are co-transported with sodium to be reabsorbed in the proximal tubule. Increased delivery to the proximal tubule = increased reabsorption of sodium = decreased delivery of sodium to the macula densa = autoregulatory mechanisms to increase sodium delivery to macula densa to maintain steady state = increased renal blood flow Similar mechanism may explain the **marked increase in flow in uncontrolled hyperglycaemic states**

Answer 37

~ 60% of kidney function lost

Answer 38

* Prevention * Low phosphate diet * Phosphate binders * - calcium. Can result in total body calcium accumulation * - sevalamer and lanthanum. Don't predispose to hypercalcaemia * Calcitriol * - direct **suppression of PTH secretion** * - **indirect suppression of PTH** secretion by raising ionized calcium concentration * - can result in **hypercalcaemia/hyperphosphataemia through GIT absorption** * **Calcimimetics** * - cinacalcet * - enhance sensitivity of parathyroid cells to suppressive effects of calcium * - reduce PTH and plasma calcium

Answer 39

**Systemic disorder resulting from mutations in PKD-1/2 genes** * both transmembrane proteins in all segments of the nephron * 1:400-1000, accounting for 4% of ESRF * 90% inherited, remainder spontaneous * PKD-1 85% and worse prognosis **Presentation** * significant phenotypic heterogeneity * often asymptomatic until 4th-5th decade, with slow decline in function over 10-20yrs * abdo pain, haematuria, UTI, hypertension, masses, renal impairment, imaging * rupture can result in gross haematuria or acute pain with signs of peritonitis * increased frequency of UTIs and cyst infection can occur Diagnosis * Family history or imaging studies * genetic analysis for PKD-1/2 in equivocal or considering family donor * Screening for aneurysms only in FHx, intervene for \>10mm **Extra-renal manifestations** * Cerebral aneurysm: 2-4x increased risk of SAH from rupture. Highest risk in FHx of aneurysm * Hepatic cysts: 50-70% by age 60, weakly correlated with extent of renal disease * Pancreatic cysts: 7-10% * Cardiac disease: valvular disease in 25-30%, most commonly MVP/AR * Diverticulae and hernias: increased frequency and incidence of colonic perforation

Answer 40

Heavy proteinuria Minimal haematuria Hypoalbuminaemia Hypercholesterolaemia Oedema Hypertension

Answer 41

Makes up **70-90% of nephrotic syndrome in childhood** * only 10-15% in adulthood * can be a misdiagnosis of early **FSGS** (if you miss the sclerosed glomeruli on your biopsy), consider in those non-responsive to steroids or frequently relapsing **Associations** * hodgkins * allergies * NSAIDs * URTI **Pathology** * - Nothing on light microscopy and nothing on immunoflourescence * - Effacement of foot processes on electron microscopy **Presentation** * Abrupt onset of oedema and nephrotic syndrome with acellular sediment * Hypertension in 50%, atopy/allergies in 30% * Decreased GFR in 30%, predictors: low serum albumin and intrarenal oedema. Responds to IV albumin and diuretics * Can get ATN and interstitial inflammation **Treatment** * **Prednisolone first line. Not resistant until after 4 months** * 80-85% CR by 20-24 weeks. *Increased relapse with rapid taper* * Cyclosporine can induce remission * Cyclophosphamide, chlorambucil, MMF in relapsers, steroid dependent, steroid resistant **Prognosis (in those who are steroid responsive)** * 50-75% have a relapse * 10-25% have frequent relapses * 25-30%steroid dependent

Answer 42

Segmental glomerular scars involving some but not all glomeruli * most prominent in glomeruli at the corticomedullary junction (superficial biopsy can miss it) * 4 histological variants **Epidemiology** * ~1/3 of adult nephrotic syndrome * 1/2 of **African Americans** **Causes** * Primary FSGS * Secondary FSGS - viruses, hypertensive nephropathy * reflux nephorpathy * cholesterol emboli * drugs * sickle cell disease, lymphoma, radiation nephritis **Adverse predictors** * Nephrotic range proteinuria * African American * Renal insufficiency * fibrosis on biopsy **Treatment** * Primary: steroids work but less often than in MCD. Remission in 20-45% on steroids for 6-9 months * Cyclophosphamide in steroid non-responsive (30-50% respond) * cyclosporine works but is itself nephrotoxic and they relapse when it's stopped * **Secondary: no evidence for immunosuppression, just treat the cause** * Recurs in 25-40% of transplants for ESRF with graft loss in 50% of those

Answer 43

Accounts for **~30%** of **nephrotic syndrome** in adults * - Most common cause in the elderly and in Australia * - Peak 30-50; M:F 2:1 **Aetiology** * most commonly idiopathic * 25-30% associated with: malignancy, infection, rheumatologic conditions * Need to distinguish from diabetes and amyloidosis **Pathology** * strongly associated with **IgG4 subtype deposition** * **M-type phospholipase A2 receptor antibody (** associated with idiopathic, titre of antibody correlates with disease severity * **Positive in 70-80% of idiopathic membranous** nephropathy, primarily **IgG4** subclass * **_antibody response to treatment correlates with disease response_** * **_'Spikes' on silver staining (membrane growing around immune deposits)_** * **_anti THSD7a present also_** Subendothelial deposits or tubuloreticular inclusions points strongly toward membranous lupus nephritis **Prognosis** * 1/3 spontaneously remit, but not necessarily quickly * 1/3 have relapsing nephrotic syndrome with normal renal function * 1/3 develop renal failure or die due to complications of nephrotic syndrome * has the **highest incidence of thrombosis of the nephrotic syndromes** * warfarin if serum albumin \<20mg/day * adverse predictors: male, \>50yrs, hypertension, proteinuria **Treatment (steroids alone don't work)** * **Cyclosporin effective** in inducing remission but **relapse commo**n after cessation * Risk of long-term continuation at low dose unclear * **Rituximab (MENTOR)** –as _**effective as cyclosporin** in inducing remission and **remaining relapse-free;** increasing evidence;_ * not on PBS for membranous nephropathy * What we don’t know how rituximab compares with cyclophosphamide require further studies * Generally a period of non-immunosuppressive period for spontaneous remission * Don’t forget: * Anticoagulation (**higher VTE risk for same level of hypoalbuminaemia**); * Statin; Diuretics & salt/fluid restriction

Answer 44

* *X-linked inborn error of globotriaosylceramide metabolism** (lysosomal storage disorder) - lysosomal **_alpha-galactosidease A activity_** **Present in 3rd decade with** * mild-mod proteinuria -\> progression to ESRF * skin lesions (angiokeratomas) * neurologic: **acroparasthesia** due to small-fibre neuropathy * **cardiac: LV enlargement,** conduction abnormalities * *Maltese cross fat globules under polarized light in the urine** - due to accumulation of non-broken down stuff **Treatment** * - RAAS * - recombinant alpha-galactosidase A clears the deposits

Answer 45

Distal tubule - Principal = Na and H2O. Affected by ADH - Intercalated = K and H

Answer 46

Acute kidney injury characterised by **inflammatory infiltrate in the renal interstitium** **Causes** * **Drugs: 70-75%;** abx 30-49%; NSAIDs; others * Infections: 4-10% * **Systemic diseases:** 10-20%. Sarcoid, sjogren's, SLE, MM * Tubulointerstitial nephritis and uveitis syndrome: 5-10% **Presentation** * Nonspecific symptoms * Usually without proteinuria, more common in NSAID induced * Rash, fever, eosinophilia (triad in10%) **Ix** * - *_Temporal relationship to cause_* * - Inflammatory sediment: RBC, WCC, WCcasts * - no single investigation is diagnostic, it's a **clinical diagnosis with supportive investigations**

Answer 47

**_IgA nephropathy_** * Peak 20-30yrs, M:F 2:1, highest in Asians/Caucasians * also the commonest GN causing ESRF or transplant **Pathology** * Unclear aetiology (thought that it it's due to IgG antibodies against glycosylated region of IgA -\> IgA-IgG ab complex deposition) * Mesangial deposition of IgA (plus others)-\> reaction -\> injury **Presentation** * 40-50% \>=1 *macroscopic haematuria,* during or immediately post **URTI** * 30-40% microscopic haematuria during or immediately post URTI * \<10% nephrotic syndrome or RPGN **Associations** * CLD, especially alcohoic cirrhosis: most common secondary IgA nephropathy **Diagnosis** * **Renal biopsy:** Prominent, *globular deposits of IgA, often with C3 and IgG in the mesangium* * *Indistinguishable from HSP*; SLE has more IgG **Prognosis** * 50% slowly progress to ESRF over 20-25yrs * Predictors of progressive: serum creatinine, new HTN (5x higher progression c/w normotensive), persistent \>1g/day protein (5x higher progression c/w \<1g/day), smoking, hyperlipidaemia, ACE genotype DD * In IgAN, **even \> 1 g/day proteinuria associated with poor renal prognosis** * **Asians (Chinese)** – increased risk of more rapid progression * **Frank haematuria = good prognosis** **Treatment** * BP control, **RAAS if proteinuria (essential first line treatment), statin if lipids** * Isolated haematuria with no/minimal proteinuria = don't treat, don't biopsy. Monitor 6/12 * Persistent proteinuria = RAAS * Severe/RPGN with nephrotic range proteinuria or severe findings on biopsy = immunosuppress * no evidence it's of benefit and some that it's of harm but feel like something should be done * - steroids + cyclophosphamide followed by azathioprine

Answer 48

*_Calcium free associated with a 22% reduction_* in all cause mortality. * sevalamer has more safety data than lanthanum Should only use **calcium based i**n * **hypocalcaemic/normo**calcaemic **without vascular calcification** or adynamic bone disease

Answer 49

**Phosphate (high = bad)** * HR ~2 for \>2.0mmol/L **Serum albumin (low = bad)** * HR 3.4 for 30-34 * HR 7 for 25-29 * HR 13 for \<25

Answer 50

* Stimulates aldosterone secretion -\> **Na reabsorption** in distal tubules * Constricts **efferent arterioles** -\> Increased **Na reabsorption** * Efferent artiorole constriction *reduces peritubular capillary hydrostatic pressure,* favouring **reabsorption** * Efferent arteriole constrictio*n increases peritubular capillary colloid osmotic pressure,* favouring **reabsorption** * **Direct stimulation of Na reabsorption** * In proximal, loops, distal, collecting * Alters the **pressure-natriuresis curve (see attached)** * Normal curve is very steep, meaning minor changes in BP increase Na excretion * HTN with impaired ability to decrease renin excretion lose curve steepness, requiring much higher BP to increase Na excretion * **Angiotensin II blockade shifts the curve to the left, allowing for lower BPs to excrete Na**

Answer 51

**Angiography higher risk than contrast CT** **Risk factors** * - CKD * - Diabetic nephropathy higher risk than other CKD * - Heart failure, due to renal hypoperfusion * - MM * - hypoosmolar contrast (not used in Aus) **\<1% go on to require dialysis** **Risk management** * - Don't use contrast * - Use a lower dose and avoid repetitive studies * - Avoid volume depletion and NSAIDs * - Hydrate: 8hourly bag NaCl 0.9% running 8hr pre until 8hrs post * - NAC carries risk of anaphylaxis and has conflicting data * **- Prophylactic haemofiltration** works but not done outside of those **_already being dialysed_**

Answer 52

Have to **discontinue antimetabolite** * **- azathioprine or MMF** * - essential for virus eradication Shouldn't stop calcineurin inhibitor

Answer 53

* *Fractional sodium excretion** - Urine **sodium is low** (\<20mEq/L) in **pre-renal disease** due to conservation of Na and water - Urine **sodium is high** (\>40-50mEq/L) in **ATN due to impaired tubular reabsorption** **Limitations** * Can be low in ATN superimposed on chronic pre-renal disease * Low fractional excretion of sodium **not unique to pre-renal disease** * Diuretics make it a free for all **Other** * Fluid responsiveness: If back to normal within 24-72 hrs post repletion then pre-renal, otherwise ATN * BUN/Cr ratio: normal (10-15:1) in **ATN; \>20:1 in pre-renal**

Answer 54

Pigmented granular casts in the urine Red/brown colour of urine Marked increase in CK Can be differentiated from haemolysis by * haptoglobin * peripheral blood smear

Answer 55

Concentrates in the proximal tubular cells Preferentially accumulates in the renal cortex - concentration can greatly exceed that of serum

Answer 56

**No difference** in survival or CV events/infections/dialysis complications * 828pts assigned to dialysis at eGFR 10-14 vs 5-7 **Absolute indications** * Uraemic pericarditis/pleuritis/encephalopathy * No correlation between urea level and manifestations, has more to do with rate of accumulation **Common** * Declining nutritional state * Refractory acidosis, hyperkalaemia, hyperphosphataemia * Persistent or difficult to treat volume overload **eGFR of 5-15 is the grey zone** * \>15 generally don't * \<5 generally unable to be treated medically * 5-15 judge based on symptoms

Answer 57

Aim **Tsat \>20%** and **ferritin \>200-300** * **- IV superior to oral in dialysis patients** In HDx IV is preferred **with dialysis** In PD or pre-dialysis **subcut is preferred weekly/fortnightly** Most common side effect is **hypertension** * - 20-50% will develop DBP \>=10mmHg Many others, but headache, rash and flu like syndrome common **Pure red cell aplasia is rare** * - Due to antibodies against EPO molecule * - Consider in those with significant anaemia in EPO \>=3-4/52 that's previously responded

Answer 58

* *_FGF-23_** can indicate need for intervention even in normal phosphate levels - secreted by osteocytes - increases early in the course of CKD - results in internalisation of the sodium phosphate cotransporter in the proximal tubule -\> phosphaturia Increases renal phosphate excretion Stimulates PTH which also increases phosphate excretion Suppresses formation of 1,25OHD, leading to diminished phosphate absorption in the GIT

Answer 59

Living donor trumps deceased donors * ABO incompatible tranbsplant simjjilar longterm outcome incontemporary era - increased death-censored graft loss and rejection in first month * *3/6 HLA matched family donor** beats randomly selected cadaveric donor * *0/6 HLA match in both living and deceased** confers **poor outcomes** Living unrelated as high as 6/6 HLA match deceased and comparable to living related * *Increased survival with decreased age of deceased donor** - No absolute upper limit for donation - Survival of allografts from \>70yrs is lower than from younger

Answer 60

* *Renal disease** - \>80% with CRF/CKD have hypertension - more severe in glomerular disease than interstitial

Answer 61

Due to an occlusive ledion of a renal artery --\> underlying **mechanism is activation of RAAS** **Groups** * Older arteriosclerotic patients with an obstructing plaque * Fibromuscular dysplasia: more common in young, white women. Often bilateral and more distal **Consider** * Other evidence of atherosclerotic vascular disease * Recent loss of hypertensive control, unexplained deterioration in renal function or decline with ACEI * 50% have an abdominal/flank bruit **Ix** * DTPA can look at flow. Not useful in bilateral or eGFR \<20 * Doppler U/S provides good estimates of flow * Angiography the gold standard

Answer 62

**Pre-renal** * Most common form of AKI * Usually due to decreased CO; autoregulatory mechanisms fail at SBP \<80 **Intrinsic** * Sepsis: complicates \>50% sepsis; can occur without hypotension * Ischaemia * Nephrotoxins: contrast, abx (ATN vs AIN), chemotherapy, endogenous **Post-renal** * Manifold

Answer 63

**Below account for \>90%** * Diabetic nephropathy * Glomerulonephritis * HTN-associated CKD * Autosomal dominant polycystic kidney disease (ADPKD) * Other cystic and tubulointerstitial nephropathy

Answer 64

**Renal PCTs increase production of NH3 from breaking down glutamine** * Then secreted into the urine where it buffers H and allows for net excretion of acid * (NH4+ can't cross back across into the tubular cells)

Answer 65

Glucocorticoids **accelerate recovery but don't impact survival**

Answer 66

therapeutic agents, infection, autoimmune + acute obstructive disorders

Answer 67

Due to **crystal deposition** in **tubular cells and interstitium** **Sulfadiazine for toxoplasmosis** **Indinavir or atazanavir for HIV IV aciclovir** **Findings** * **'sheaf of wheat'** sulfonamide crystal * *reg-green birefringent needly shaped crystals* of aciclovir

Answer 68

**Recurrent UTIs** * with subsequent **patchy interstitial scarring and tubular atrophy** * loss of functioning nephrons with hypertrophy of the remnant glomeruli * **eventual secondary FSGS** **U/S** * asymmetric, small, irregular kidneys with thin cortices Surgical reimplantation not of help in adults after damage is already done

Answer 69

**Slowly progressive kidney disease** * Accumulates in the principal cells of DCT by entering through epithelial Na channel * Inhibits glycogen synthase kinase and downregulates vasopressing-regulated aquaporins * Can get chronic tubulointerstitial nephritis after 10-20yrs. More in those with repeated toxicity **Treatment** * amiloride inhibits entry into the principal cells * Frequent monitoring. Discontinuing can be difficult.

Answer 70

* *Multifocal FMD i**s more common - **String of beads** on **angiography** - Corresponds to **medial fibroplasia** * *Focal FMD** - **Circumferential or tubular stenosis** on angiography - Corresponds to **intima fibroplasia**

Answer 71

**Fibromuscular dysplasia** * responds well to **percutaneous renal artery angioplasty** **Atherosclerotic renal artery stenosis** * if BP controlled and renal function stable can be **_medical managed_ and followed up** **Medical** * RAASI, cease smoking, statins, aspirin **Revascularisation** * Reserved for failing medical therapy or developing complications * Complications: dissection, capsular perforation, haemorrhage, atheroembolic disease * Flow restored in 25%, no change in 50%

Answer 72

**Cholesterol crystals** breaking free from **atherosclerotic plaque** lodging in **downstream microvessels** * mostly after *angiographic procedures of coronary vessels* **Other causes** * **vascular surgery** * anticoagulation with heparin * thrombolysis * trauma **Risk factors** * diabetes, HTN, IHD **Clinical** * 1-14/7 after event, can continue **for weeks after** * **fever, abdo pain, weight loss, cutaneous manifestations** (livedo reticularis, localised gangrene) * **transient eosinophilia** common, increased ESR, decreased complement * biopsy shows **microvascular occlusion with cholesterol crystals** **Treatment** * nothing effective once developed * withdraw anticoagulation * statins might help

Answer 73

The name given to those wit**h ESRF without a specific aetiology** * afferent **arteriolar thickening** * **homogenous eosinophilic deposition** * **narrowing of vascular lamina** **Clinical** * LVH * HTN * retinal hypertensive changes **Management** * antihypertensives help CV outcomes but not course of kidney dysfunction

Answer 74

Occlusion of the **vasa recta** in the renal medulla * relative hypoxia predisposes to **_HbS_ polymerization and erythrocyte sickling** **Sequelae** * hyposthenuria (low specific gravity) * haematuria * papillary necrosis **Proteinuria in 20-30%** * treat with **ACEI**

Answer 75

**_Type 1_** * - **Defect in DCT intercalated hydrogen excretion**. Antiporter with K explains hypokalaemia. * - Can get **very acidotic** * **- Stones due to multiple mechanisms:** * - Increased bone release of calcium/phosphate to buffer acidosis * - Direct reduction in tubular reabsorption of calcium/phosphate * - High urine pH favour calcium phosphate precipitation (but not calcium oxalate) * - Decreased citrate excretion (usually a potent inhibitor of calcium stone formation) **Causes** * - Autoimmune: **Sjogren's, AIH/PBC, SLE, RA** * - Drugs: **Amphoteracin B, lithium, ibuprofen** * **- Hypercalciuria** * - Other: Wilson's, obstructive nephropathy, renal allograft rejection **Treatment** * - Underlying cause and **bicarbonate - alkali therapy** * - Reduced hypokalaemia and nephrocalcinosis/stones/OP **_Type 2_** * - Defect in proximal bicarbonate resorption; once serum matches resporptive capacity the urine become bicarb free * - Classic Fanconi: generalised proximal tubular resorptive defect * - Acidosis stabilises due to residual resorptive capacity of tubules * - Hypokalaemia due to mild hypovolaemia resulting in hyperaldosteronaemia * - Treatment can worsen due to increasing sodium and water delivered to distal tubule. Overcome by replacing alkali with potassium citrate **Causes** * acetazolomide * monoclonal gammopathies **Treatment** * Underlying cause * Much higher bicarb doses - note that hypokalemia WORSENS with therapy * Thiazide (induces mild hypovolaemia -\> proximal sodium and thus bicarb resorption) **_Type 4_** * - Hypoaldosteronism or aldosterone resistance -\> i**mpaired H and K secretion** * **- Hyperkalaemia** -\> intracellular alkalosis due to exchange of K with H -\> reduced NH3 secretion in the proximal tubule -\> decreased urine buffering and acid excretion * - Low urinary pH due to inadequate NH3 for buffering. Different to type 1 where the H that gets through in the urine can be buffered by NH3 and allows for alkalotic urine **Causes** * Reduced aldoserone production * aldosterone resistance

Answer 76

**Kt/V** * *Clearance of urea multiplied by duration of dialysis divided by volume of distribution of urea in the body* **Issues** * - Need to wait for urea to equilibrate due to recirculation * *- Urea clearance may not reflect other toxin clearance* * - Presumes a single session represents all sessions

Answer 77

**No.** HEMO showed no difference in haemodialysis, ADEMEX showed no difference in peritoneal dialysis

Answer 78

* *Yes.** ESRDCPM showed tha**t mortality was increased on the day following the long interval on 3x weekly haemodialysis** - 22.1 vs 18.0 deaths per 100 person years

Answer 79

**Sessions \>240mins** associated with **increased survival** **Fluid balance** * Being \>2kg over or \>2kg under dry weight consistently is associated with increased mortality compared to hitting dry weight **Dry weight =** the minimum sodium and volume that can be tolerated without inducing hypotension

Answer 80

**Inadequate ultrafiltration** associated with **increased mortality** **Ultrafiltration \>12mL/hr/kg** associated with **increase CV mortality**

Answer 81

o**AV fistula + Hb \>=110 + goal albumin level**

Answer 82

**_\<5%_** **Risk factors** * Prior sensitisation with \>50% panel reactivity * Presence of delayed graft function (DGF) * Requirement for dialysis within the first week after transplantation * Number and severity of rejection episodes * 2nd/3rd transplant * **Donor \<5yrs or \>60yrs** * Greater degrees of **HLA mismatching** * **Allograft disfunction at discharge (\>176mmol/L)**

Answer 83

**Immediate** * **Pre-renal:** hypotensiona and volume depletion * **Renal:** Post-ischaemic ATN most common. Hyperacute/acute rejection less so (acute = \>24hrs post) * **Post-renal:** Obstruction: ureteral necrosis + leak/haematoma **Early (1-12 weeks)** * Pre-renal is same * Renal: Rejection most common, cellular or antibody mediated, 20% get it, usually \<6 months and often early. Hypertension common, creatinine rise late. * **Calcineurin inhibitor toxicity:** acute = arterioles and responds to reduction. chronic = endothelial damage and doesn't respond * Post-renal: obstruction **Late (\>3 months)** * Pre-renal: volume and renal artery stenosis * Renal: Rejection, calcineurins, recurrence of primary disease, de-novo disease * Post-renal: Obstruction **Late chronic** * Chronic allograft nephropathy, acute rejection is a major predictor * Calcineurins * Hypertensive nephrosclerosis * Viral * Recurrent or de-novo disease

Renal Flashcards

(130 cards)