class: RWH_bg_title # .black[Renal QI] ### Quite interesting renal cases .RWH_footnote_title[ .RWH_footer_bold[ Rob Hunter | @renalrob ] ] .RWH_footnote_right_title[ .RWH_footer_bold[ 20th Jan 2023 ] ] ??? GIM lunchtime teaching 20th May Literally quite interesting Created with [xaringan](https://github.com/yihui/xaringan). --- class: center, middle, inverse *NB all of the cases in this presentation have been redacted to remove patient identifiable information* *the only remaining slides are for the discussion / learning points* --- class: center, middle, inverse # .white[Case 1] ### 67M with AKI --- # Case 1 - learning points ### Obstruction - sometimes polyuria (tubular injury) - if low pre-test probability, USS can rule out; not so if high - **obstruction with hydronephrosis** = volume depletion, retroperitoneal pathology (fibrosis, cancer) - **hydronephrosis without obstruction** = profuse diuresis (NDI), pregnancy, early post-obstruction - good recovery up to 1 week; poor after 12 weeks (for complete obstruction) --- class: center, middle, inverse # .white[Case 2] ### 40M with blurry vision ---  .RWH_footnote_right[.RWH_footer_style[Ettehad (Lancet 2016)]] ??? Meta-analysis of 123 trials with 600,000 participants. --- # Case 2 - learning points ### HTN - for most people, anti-hypertensives do not prevent progression of CKD... - ...but in selected cases they do (heavy proteinuria, risk of hypertensive emergency) - susceptibility if Black African family origin --- class: center, middle, inverse # .white[Case 3] ### 69M with AKI and heart failure --- # Case 3 - learning points ### 'AKI' in heart failure - difference between spontaneous and induced 'AKI' (or 'WRF') - role of venous congestion - diuretic strategy in decompensated heart failure ??? WRF = permissive hypercreatininaemia --- <!--    -->  <br> - down shift in heart failure - right shift in CKD - effects of gut oedema - log scale .RWH_footnote_right[.RWH_footer_style[Ellison & Felker (NEJM 2019)]] ??? Ellison & Felker (NEJM 2019) and Braunwald (EHJ 2014): - down-shift in CCF due to RAS + / SNS + / DCT hypertrophy - right-shift in curve due to renal insufficiency (reduced secretion) - ...NB log scale - hence why we double doses in resistance - gut oedema doesn't affect total amount absorbed but does slow absorption and so blunt the peak - NaCl intake should be low to allow excretion to exceed intake (periods of anti-natriuresis) ---  <br> Composite of death, re-hospitalisation, A&E visit within 60 days (pre-specified 2ry endpoint). .RWH_footnote_right[.RWH_footer_style[DOSE (NEJM 2011)]] ??? n = 300: factorial low (IV dose = N oral) vs. high (2.5x oral) and bolus vs. IVI Co-primary end-points of symptom score and SCr at 72 hrs (= 3 days). Not powered to detect hard clinical endpoints. No difference between bolus or infusion. Higher dose had better symptom control, greater diuresis, more transient SCr rises (not reaching p < 0.05). ---  <br> Change in Cr over 72 hrs (NB 0.05 mg/dl = c. 5 `\(\mu\)`M). .RWH_footnote_right[.RWH_footer_style[DOSE (NEJM 2011)]] ??? Cr went up a tiny bit (0.05 mg/dL = 5 mcM) in all but no difference between groups. ---  <br> Threshold = 20% change in eGFR (or c. 25 mcM). .RWH_footnote_right[.RWH_footer_style[DOSE re-analysis (JCF 2016)]] ??? Association of linear change from baseline over 72 hrs with outcomes over 60 days. ---  .RWH_footnote_right[.RWH_footer_style[CARESS-HF (NEJM 2012)]] ??? n = 188. More serious adverse events in the UF group (72% vs 57%) - mainly renal failure / bleeding / line-related. --- class: center, middle, inverse # .white[Case 4] ### 44F with joint pains and night sweats --- # Case 4 - learning points ### Instrinsic renal disease - multisystem disease plus abnormal urinalysis = instrinsic renal disease --- class: center, middle, inverse # .white[Case 5] ### 44M with covid --- # Case 5 - learning points ### Nephrotic syndrome - always check a uPCR / uACR if any sniff of kidney problem - secondary causes of nephrotic syndrome - Black African family origin: oedema / ApoL1 ??? Variants protective against trypanosomiasis in heterozygote state. 15% AAs hom / compound het. Spectrum of ApoL1 disease from arterionephrosclerosis (case above!) > collapsing GN. Viral trigger for collapsing GN > IFN response > TRIs. (HIV) --- class: center, middle, inverse # .white[Case 6] ### 68F with Cr 600 `\(\mu\)`M and anaemia --- # Case 6 - learning points ### ESKD - CKD *vs.* AKI - can present with ESKD - indications for RRT - risks of RCC --- class: center, middle, inverse # .white[Case 7] ### 71M with AKI and hyponatraemia --- # Case 7 - learning points ### Causes of hypoNa with normal POsm i) pseudohyponatraemia = ISOtonic: .orange[*hyperlipidaemia, paraproteinaemia, IVIg*] ii) additional effective osmole = HYPERtonic ('translocational'): .orange[*glucose, mannitol, glycine*] iii) additional ineffective osmole = HYPOtonic: .orange[*EtOH, urea, ethylene glycol*] <br> **i) and ii)** provide an explanation for the hypoNa; no risk of cerebral oedema **iii)** hypoNa not explained; risk of cerebral oedema ??? ### Clinical notes Pseudohyponatraemia caused because serum is diluted prior to analysis - so still seen with contemporary ISE methods (although was even worse in era of flame photometry). Can detect this by running a sample through ABG machine (as this uses an undiluted sample, so Na will be normal if pseudohypoNa) - see [European guidelines](https://pubmed.ncbi.nlm.nih.gov/24569125/). Glycine encountered in gynaecological / urological irrigation fluids - e.g. TURP syndrome. The risk of cerebral oedema is not elevated in i) and ii). The risk of cerebral oedema is high in iii) because serum tonicity is LOW - even when osmolality is high. <br> ### Basic concepts See [European guidelines](https://pubmed.ncbi.nlm.nih.gov/24569125/), [KI quiz](https://doi.org/10.1016/j.kint.2020.03.006) and [JAMA review](https://pubmed.ncbi.nlm.nih.gov/10030305/). Remember [basic definitions](https://derangedphysiology.com/main/cicm-primary-exam/required-reading/body-fluids-and-electrolytes/Chapter%20012/osmolarity-osmolality-tonicity-and-reflection-coefficient): - osmolality (or better "osmotic concentration") = number of solute particles per unit volume - tonicity = osmotic pressure between two compartments (a function of the effective osmoles - i.e. the osmolar concentration and the properties of the semi-permeable membrane) - reflection coefficient = a measure of how well a solute passes through a membrane (1 = impermeable; 0 = completely permeable) - effective osmole = unable to penetrate the membrane - ineffective osmole = able to freely cross the membrane Na, K etc. are effective osmoles. EtOH is an ineffective osmole (reflection coefficient for EtOH ~ 0). Urea is intermediate. Is hydrophobic and so doesn't cross lipid bilayers; reflection coefficient depends on expression of urea transporters. Reflection coefficient for urea ~ 0 for skeletal muscle and ~0.5 for the cerebral capillaries. Therefore rapid changes in urea can cause cerebral oedema (e.g. in dialysis equilibrium) - but for the purposes of evaluating hypoNa, can consider urea as an ineffective osmole (as will have equilibrated when not changing rapidly). See [Sterns](https://doi.org/10.1038/ki.2014.320) and [Halperin](https://pubmed.ncbi.nlm.nih.gov/8712203/) reviews. NB Urea is [an effective osmole in the distal nephron](https://doi.org/10.1159/000503773) - hence its utility in treating SiADH. --- # Case 7 - learning points ### Causes of hypoNa with normal POsm Clinical pearls: - check a sample on gas machine to pick up pseudo-hypoNa - check EtOH levels (and divide by \~4 to convert mg/dL to mOsm) ??? At one point, was thought that the contribution of EtOH to Osm may be higher than its molar concentration - so conversion factors of 3.7 -- 4.0 used. However, this was based on flawed reasoning, so [it is in fact correct to convert based on its molar concentration](https://doi.org/10.3389/fmed.2019.00306) (i.e. divide by 4.6 as MW is 46 g/mol). In practice, easiest to remember by dividing by 4 to approximate. --- # Case 7 - learning points ### Causes of an elevated OG (> 10 mOsm) **Without** acidosis: - EtOH \* - pseudohypoNa - radiocontrast, mannitol, glycine, IVIg With **metabolic acidosis**: - toxic alcohols (with WAGMA - NB OG falls as AG increases) - propylene glycol infusion - and perhaps (small OG) with lactic acidosis, ketoacidosis \* and CKD \* *can get EtOH with acidosis in alcoholic ketoacidosis* ??? See [UpToDate](https://www-uptodate-com.ezproxy.is.ed.ac.uk/contents/serum-osmolal-gap?search=osmolar%20gap&source=search_result&selectedTitle=1~32&usage_type=default&display_rank=1). --- # Case 7 - learning points ### Causes of hypoNa in EtOH - hypovolaemia (50 %) - pseudohypoNa from hyperTRIGs (25 %) - beer potomania (10 %) - other ??? Figures from small [Greek case-series](https://pubmed.ncbi.nlm.nih.gov/11093969/). --- class: center, middle, inverse # Thank you ### .white[@renalrob]