<br>  # .black[How to assess kidney disease] FY1 Teaching May 2025 | Robert Hunter <!-- # Reflections after 2024 - to change for 2025 Now working well - could change nothing. Add in bit of maths for Plasmalyte chat: 500 ml plasmalyte = 2.5 mmol K vs. 2500 mmol (55 mmol per kg) in 50 kg = 1/1000. Could add in venous return curve and factors affecting MSFP (= filling and venous tone) for supplemental slides and also tighten up supplemental slides (better referencing). --> --- # How to assess kidney disease .pull-left[ - assessing kidney disease - common pathologies - investigations - management of AKI - prescribing - when & how to refer ] -- .pull-right[] ??? Often person on the team who will know the most AKI in 10 - 20% of hospital admissions. CKD in 10% (and therefore presumably much higher in hospital population). [750 nephrologists](https://link.springer.com/chapter/10.1007/978-3-030-56890-0_51) in UK and 250,000 doctors = 0.3%. --- # 79F with pneumonia Smoker, EtOH XS, hip replacement, HTN on two agents. Getting worse after 7 days in hospital. Not for ITU. - SCr 60 > 80 > 198 mcM | eGFR 22 ml/min/1.73m² - Na 132 mM; K 5.9 mM - Hb 102 g/L; MCV 98; WCC 13.5; plt 566 <br> -- - ABP 110/60 (after period of systolic in 90s) - JVP **not visible** unless lie flat - urine output 15 ml in past 6 hrs - poor oral intake since hospital admission; no IV fluids <br> -- - increasing **O₂** requirement (4L/min nasal) - JVP **elevated** - IVI at 250 ml/hr (**3L +ve** in 24 hrs) ??? What is her GFR? What is the best measure of current kidney function? What would you like to know in Hx and Ex? What fluids would you prescribe? How would you manage her AKI? Now what fluids would you prescribe? Why have the IV fluids not provoked a urine output? Why does she have an AKI? Does she have CKD? What investigations would you request? Would you refer to renal? <br> ### Fluids Meta-analysis (NEJM Evidence 2022); n = 35,000 balanced *vs.* saline in critical care. Likely mortality benefit but v. v. small effect size (90% likely in Bayesian analysis). Evidence of harm in traumatic brain injury. Err towards balanced crystalloids. Be aggressive in first 6 hrs (golden hours); conservative after this. Fluids are ‘thrombolysis’ for the kidney. Special circumstances: - vomiting / alkalosis - brain injury - cirrhosis - hyponatraemia - hyperkalaemia <br> ### Differential diagnosis if fluid-unresponsive: - not enough fluid (unlikely) - already too congested - fluid going into the wrong places (leaky microcirculation) - established ATN (as in this case) - blocked catheter --- # Medications - aspirin 75 mg od - amlodipine 10 mg od - atenolol 25 mg od - simvastatin 40 mg od - paracetamol 1g qds - morphine sulphate 10 mg prn 1 hrly - dalteparin 5000 units s.c. - piperacillin/tazobactam 4.5g IV tds ??? What would you do with her drugs now? What would you do with her drugs next week? --- # Referral: when & how - **when**: + approaching RRT (6 Ps) + suspected intrinsic cause <br> - **know**: + PMHx + drugs + examination findings + urine output + urine dip + why are you phoning? --- # Take-home messages - urine output = GFR now - always plot Cr (or eGFR) - blood and protein on dip = intrinsic renal disease - uACR or uPCR to quantify proteinuria (see the dog on fire) - concept of impaired autoregulation of RBF - correct hypovolaemia then stop  --- class: center, middle, inverse # .white[Reference slides] ---  ---  ---  ---  ---  ??? Images on left show capillaries in buccal mucosa in a patient with sepsis (Vincent & De Backer, NEJM 2013). Images on right show stripping of capillary glycocalyx in [rat model](https://www.nature.com/articles/s41598-024-60919-5) of sepsis. ---  <!-- .RWH_footnote_right[.RWH_footer_style[Abeulo et al (NEJM 2007)]] --> ---  <!-- .RWH_footnote_right[.RWH_footer_style[Abeulo et al (NEJM 2007)]] --> ---  <!-- .RWH_footnote_right[.RWH_footer_style[Thadhani et al (NEJM 1996)]] --> ??? ### Causes of low renal perfusion - hypovolaemia (including third-space losses) - low effective arterial blood volume (CCF, cirrhosis) - distributive causes (sepsis, hepatorenal) - drugs (ACEi, NSAIDs, CNIs) - macro-vascular obstruction (RAS, dissection, cross-clamp) - micro-vascular (accelerated HTN, atheroembolism, SRC, TMA) Think twice about drugs & sepsis (STOP) Thadhani et al (NEJM, 1996); Abeulo et al (NEJM 2007); Vincent & De Backer (NEJM, 2013) ---  ---  ---  --- # Drugs in AKI <br>  ??? Red = directly nephrotoxic Purple = accumulate in renal failure Blue = harmful when stopped and not re-started Should we stop ACEi? Should we have sick day rules? --- class: center, middle, inverse # .white[Supplemental slides] ### .white[ *Cr plot gallery* *volume assessment* *renal haemodynamics* *proteinuria* ] --- class: center, middle, inverse # .white[Cr plot gallery] ---  ??? Myeloma + contrast ---  ??? DKD ---  ??? AIN (Sjogrens) ---  ??? ATI (sepsis / ortho) ---  ??? RAS + ACEi --- class: center, middle, inverse # .white[Volume assessment] --- # Volume assessment - peripheral perfusion - peripheral oedema - JVP - blood pressure (relative & absolute) - postural changes - always helpful… - urine output (+/- catheter) - fluid balance chart - weight chart ??? Potential confounders in peripheral perfusion / postural changes… Oedema – where / semi-quantitative / absence of oedema Lie flat for JVP Relative hypotension: Liu et al (NDT 2009) --- # Tricky volume assessment .pull-left[ - sepsis - heart failure - cirrhosis - nephrotic syndrome - young people - old people - Black African family origin ] .pull-right[  ] .RWH_footnote_right[.RWH_footer_style[Vincent & De Backer (NEJM, 2013)]] --- # Tricky volume assessment - individual signs unreliable (unless at extremes – e.g. JVP < 1 or > 10 cm) - quantify oedema (can even be negative!) - almost never “intravascularly deplete but extravascular overload” - Bayesian approach <br> *EABV = “a poorly measurable quality of arterial filling determined primarily by blood volume, cardiac output, and vascular tone”* ??? Blood distributed 85 % in venous; 15 % arterial. The description “ECF overload but intravascularly deplete” is usually wrong. Rather there is reduced EABV. Studies in CCF and cirrhosis – showing overall vascular expansion but re-distribution into venous (e.g. splanchnic) circulations. --- class: center, middle, inverse # .white[Renal haemodynamics] ---  ---  ---  ??? - low Cl at MD (or NKCC2i) stimulates COX2 - PGE2 stimulates aa vasodilatation (counteracts vasopressors in volume depletion)... - ...and also renin release - hence role in maintaining glomerular perfusion in hypovolaemia - hence hyperPGE2 in Bartter ---  ---  --- class: center, middle, inverse # .white[Proteinuria] ---  ---  --- # Proteinuria - usually ignore trace results - dip ‘+’ = 30 mg/dL = PER 0.5 g/d = overt proteinuria - dip ‘+++’ = 300 mg/dL = PER 1–2 = heavy proteinuria - to convert PCR to PER, divide by 100 - ACR >220, PCR >350, PER > 3.5 g/d = nephrotic ---  ---  .RWH_footnote_right[.RWH_footer_style[https://edren.org/ren/handbook/unithdbk/ckd/proteinuria/]]