Dark purple urine secondary to Hydroxycobolamin!
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General Critical Care
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70-year-old male presents with one month of hemoptysis and shortness of breath. Acute renal failure, anemia, bilateral infiltrates on chest X-ray.
CT scan of the chest:
Kidney profile:
Bronchoscopy
The liver and kidney in pulmonary hypertension and right heart failure.ย A, Acute ischemic hepatitis and congestive hepatopathy.ย Rightย inset, Centrilobular necrosis in ischemic hepatitis.ย Leftย inset, Chronic hepatic congestion with sinusoidal dilatation and portal fibrosis.ย B, Congestive nephropathy.ย Rightย inset, Low perfusion kidney injury caused by hypoperfusion and ischemia, demonstrating fibrosis (*), necrotic cells (arrowhead), and intraluminal debris.ย Leftย inset, Congestive nephropathy, characterized by interstitial edema, swollen tubule cells, and tubular compression. ALAT indicates alanine transaminase; AP, arterial pressure; ASAT, aspartate aminotransferase; CVP, central venous pressure; LDH, lactic acid dehydrogenase; and yGT, gamma-glutamyl transpeptidase.
Systemic Consequences of Pulmonary Hypertension and Right-Sided Heart Failure | Circulation (ahajournals.org)
Biomarkers in pursuit of precision medicine for acute kidney injury: hard to get rid of customs (krcp-ksn.org)
Proposed strategies for managing AKI.
The definition of AKI encompasses an escalation in serum creatinine levels, a decrease in urine output, and the presence of kidney damage and stress biomarkers. Various biomarkers, some of which are accessible at the point of care, may assist in the early detection of AKI. These biomarkers can facilitate the timely identification of patients who exhibit potential endotypes, amenable traits for targeted interventions, or suitability for specific preventive measures. AKI subphenotypes, which are delineated by their clinical attributes, have already been integrated into routine clinical practice, including considerations such as etiology, AKI staging, severity, and duration. However, the integration of biomarkers into these subphenotypes may offer a more comprehensive and informative framework, culminating in predictive and prognostic insights. This refined definition of subphenotypes aims to distinguish patient subgroupsโฆ
Biomarkers for AKI subgroupingโdinosaur parkour illustration.
The clinical use of biomarkers in AKI is influenced by the heterogeneity of patient groups and outcomes. Biomarkers have a range of advantages, including the early detection of kidney injury, the identification of AKI subphenotypes (subsets of clinical features within a shared phenotype), the recognition of AKI endotypes (subsets of patients with distinct biological disease mechanisms), and the predictive enrichment of high-risk patient groups for specific care pathways or interventions.
AKI, acute kidney injury; CCL14, chemokine ligand 14; HJV, hemojuvelin; IL-18, interleukin-18; KIM-1, kidney injury molecule-1; NGAL, neutrophil gelatinase-associated lipocalin; PROENK, proenkephalin.
Biomarkers in pursuit of precision medicine for acute kidney injury: hard to get rid of customs (krcp-ksn.org)
Severe hydroureteronephrosis bilaterally, left greater than right. 5.1 cm complex fluid collection or mass in the left retroperitoneum possibly arising from the left kidney.
Ilofotase alfa, a human recombinant alkaline phosphatase with potential reno-protective effects, was evaluated for efficacy and safety in the REVIVAL phase-3 trial involving sepsis-associated acute kidney injury (SA-AKI) patients. The trial was a double-blinded, randomized-controlled study focusing on patients with SA-AKI, enrolled within 72 hours of vasopressor use and 24 hours of AKI onset. Its primary goal was to assess 28-day all-cause mortality, with secondary goals including the Major Adverse Kidney Events within 90 days (MAKE90), days alive and free of organ support, days alive and out of the ICU by day 28, and time to death by day 90.
The trial involved 650 patients (330 treated with ilofotase alfa and 319 with a placebo). The 28-day and 90-day mortality rates were similar in both groups (27.9% and 33.9% forโฆ
Multicenter study of hospital admissions in greater Toronto: Osmotic Demyelination Syndrome occurrence and rapid correction of serum sodium
This multicenter study which was published in NEJM Evidence this month examined 22,858 hospital admissions in greater Toronto for patients with hyponatremia (low sodium levels). Osmotic Demyelination Syndrome (ODS) occurred in a small proportion of patients (0.14%), even when they underwent rapid correction of serum sodium. The study found that rapid correction of serum sodium did not generally cause ODS, and that other unidentified factors must be involved in ODS development. Certain factors were more frequent in the ODS group, including initial serum sodium levels below 110 mmol/l, positive alcohol level, and hypokalemia. The study had several limitations, including possible lack of generalizability, missing data, and the small number of ODS patients, which limited the ability to identify specific risk factors or define safe rates of serum sodium correction. The authors concludedโฆ
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- Hussain Al-shabib
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Hydroxocobalamin chelates cyanide and forms the nontoxic, renally excreted cyanocobalamin. A common side effect of hydroxocobalamin is a stunning dark red/purple discoloration of the recipient's skin, mucosal membranes, and body fluids, including plasma and urine.
As smoke inhalation victims often demonstrate concomitant carbon monoxide and cyanide toxicities, initial blood gas measurements should be obtained prior to hydroxocobalamin administration.