C-Star Case Studies: Block D AKI-CKD - Prerenal/Intra-Renal/Post-renal. Setting: ER ID: 61-year-old female of African American Origin

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1 C-Star Case Studies: Block D AKI-CKD - Prerenal/Intra-Renal/Post-renal Setting: ER ID: 61-year-old female of African American Origin Reasons for visit: Feeling tired, with an itch all over the body HPI: Dizziness, fatigue, diffuse pruritus and decreased appetite over the 10 days PTA. The symptoms, specially the itchiness having worsened with time, interfering with her sleep in the past few days. Had a mild URTI, a cold, roughly 20 days PTA, that resolved w/o medication. Doesn t feel if there has been much of a change in urination frequency or quantity Has noticed her urine has become a bit foamy (Do not say unless specifically asked) Hasn t noticed any edema or effusion. No new medication. No recreational drug use PMHx/PSHx: Chronic sinusitis G5P3A2 (with G for total # pregnancies, P total of delivered pregnancies, A for # abortion/miscarriage, under 20 weeks), two spontaneous miscarriages Cataract surgery in left eye Med & Allergy: Allergic to Penicillin and Metronidazole (Flagyl) Takes Vitamin D and Calcium Acetaminophen p.r.n. Family history: Mother had a history of diabetes and hypertension Uncle, mother s brother, had renal failure, who had to undergo dialysis until death Father died of his second MI

2 Social History: Occasional alcohol consumption No substance use Works as a receptionist at a dentist clinic Tries to stay healthy by walking to work every day Has a son and two daughters, all three healthy Lives alone since her husband passed away roughly 2 years PTA Physical examination: General: Fatigued and pale, but otherwise well Temp: 37.1C BP: 132/68 P: 79 RR: 17 Some puffiness noticed around the eye and some pitting edema noticed in dorsum of the hand and the feet, lungs are clear and heart sounds are normal No visible rash and no other abnormality Laboratory data and Imaging: Blood test, performed 2-month PTA were normal Blood Test WBC 13.8 X 10 9 /L (4-10 X 10 9 /L) Sodium 131 mmol/l ( mmol/l) Chloride 94 mmol/l ( mmol/l) Urea 20.3 mmol/l ( mmol/l) Creatinine 885 mmol/l (50-90 mmol/l) Estimated GFR 5.06 ml/min/1.73 m² (~85 in ages 60-70) Albumin 25 g/l (35-50 g/l) Urine Dipstick positive for protein, with a few RBC Microscopic examination shows fatty casts and few monomorphic RBC On US, both kidneys appear slightly larger and the kidneys parenchyma appear hyperechoic compared to the liver, suggestive of renal parenchymal disease Differential diagnosis: AKI/ARF leading to Uremia Hypothyroidism w/ or w/o Xerosis (dry skin) Atopic dermatitis Drugs (opioids, antibiotics and anti-inflammatory, ) Malignancies (Lymphoma, )

3 Diagnosis: AKI/ARF in nephrotic syndrome, leading to Uremia (Collapsing FSGS, not associated with HIV) Notes: AKI, Acute Kidney Injury, is a sudden decline in renal function significant enough to produce uremia, and also often oliguria, a urine output of <400ml/day. It normally occurs over a period of days or week, and is often reversible. AKI can be a medical emergency and can cause death and diagnosis is usually based on serum urea and/or creatinine levels. Causes: AKI can be divided into three main categories: prerenal, intra-renal and post-renal. Prerenal causes are often due to an impaired blood flow to the kidney. This can be due to a variety of underlying etiologies, and can be a result of hypovolemia, BP, CO, vascular disease, or a combination of any of these. Possible clinical signs include history of blood/fluid loss, sepsis leading to vasodilation, cardiac disease, postural hypotension, weak, rapid pulse and low JVP Intra-Renal causes, often due to damage to the renal tubules or the glomeruli. A common example would be acute tubular necrosis where toxicity and/or ischaemia results in GFR. Other examples include nephrotoxicity due to medications, such as aminoglycosides or contrast nephropathy and renal parenchymal disease. Post-renal causes, occurring often as a result of an obstruction in the urinary tract, below the kidneys, resulting in blockage and build up in the kidneys. Examples would include kidney stones, enlarged prostate and bladder dysfunction. Investigations would include urine dipstick, urine microscopy looking mainly for hematuria, red cell casts and proteinuria and blood tests, as well as kidney function monitoring through urine output analysis. Management: Replace fluids, if hypovolemia and/or hypotension are suspected, but be careful as in many cases, prerenal and intrarenal causes can co-exist, and overloading the patient with fluids can result in massive edema. If present, treat Hyperkalemia, as soon as possible, to avoid possible complications such as arrhythmias and manage acidosis, with sodium bicarbonate, which will also help to lower free potassium levels. Consider dialysis if there is pulmonary edema, persistent hyperkalemia, severe metabolic acidosis or severe uremia causing encephalopathy or pericarditis. Remember: In the elderly, a combination of low muscle mass, and low dietary meat intake can result in a falsely low creatinine, masking AKI.

4 CKD, chronic kidney disease, is a more long term and, as the name suggests, deteriorating reduction in renal function. It is often irreversible and generally appears over a period of years. CKD progresses, to finally reach a stage where death becomes imminent in the absence of renal replacement therapy (hemodialysis, kidney transplant, ), and is referred to as end stage renal failure. Common causes include hypertension, congenital renal anomalies such as PKD (polycystic kidney disease), renal artery stenosis, glomerular diseases, interstitial diseases, systemic inflammatory diseases and diabetes. CKD has 5 stages, based on the level of dysfunction and GFR, with symptoms usually appearing at stage 4; with stage 1 being some damage with normal GFR and stage 5 being kidney failure.

5 Short Case - Diabetic Ketoacidosis 32M, presenting with tachypnea RR34, shortness of breath, use of accessory muscles, fatigue, coughing, fever and chest pain while breathing. Diagnosed with pneumonia. He has a history of type 1 diabetes, previously controlled with insulin injections. Only mention if asked: He also feels rather thirsty, but can t drink much as he also feels nauseous. He wasn t able to take his last insulin injection. Labs: ph 7.18 ( ) Serum Bicarbonate 13.7 mmol/l (24-30 mmol/l) Arterial PaCO2 29 mmhg (35-45 mmhg) Arterial PaO2 53 mmhg ( mmhg) Arterial SaO2 87% (96-100%) Blood Glucose 25.5 mmol/l ( mmol/l) Serum Sodium 134 mmol/l ( mmol/l) Serum Chloride 95 mmol/l ( mmol/l) Serum Potassium 4.1 mmol/l ( mmol/l) Serum Creatinine 97 mmol/l ( mmol/l) Urinalysis positive for ketones Diagnosis: DKA following an infection, causing metabolic acidosis with inadequate respiratory compensation Notes: Diabetic ketoacidosis, DKA, is characteristically associated with type 1 diabetes, but can also occur in type 2 diabetes, under conditions of extreme stress such as serious infection, trauma, cardiovascular or other emergencies. It is more common in young (<65 years) patients, whereas another hyperglycemic state condition called hyperosmolar hyperglycemic state (HHS) is more prominent in individuals older than 65 years. Insulin deficiency, and/or resistance, and to a lesser extent glucagon excess, are the two most important abnormalities, largely responsible for the development of diabetic ketoacidosis (DKA) and hyperosmolar hyperglycemic state (HHS), primarily in individuals with uncontrolled or NYD, not yet diagnosed, diabetes. In addition, as it s often the case while under physiological stress, increased secretion of catecholamines and cortisol, which oppose the actions of insulin, also contribute to the increases in glucose and ketone acid production. The deficiency in insulin is more severe in DKA compared with HHS. Since suppression of lipolysis and ketogenesis is more sensitive to insulin than the inhibition of gluconeogenesis, the residual insulin secretion and its systemic activity in HHS is sufficient to minimize the development of ketoacidosis but

6 not adequate to control hyperglycemia. DKA and HHS are two extremes in the spectrum of hyperglycemic crisis, and patients can present anywhere along the continuum of diabetic metabolic derangement. Management: Diabetic ketoacidosis is usually treated with fluids, insulin and electrolytes such as sodium, potassium and chloride. While left untreated diabetic ketoacidosis can lead to loss of consciousness and, eventually death, the treatment is not without its own risks and should therefore be administrated carefully. Some possible complications are hypoglycemia, hypokalemia and cerebral edema if the blood sugar level is too quickly adjusted. Extra information: Anion Gap Metabolic Acidosis: MUDPILERS Methanol - Uremia - DKA/Alcoholic KA - Paraldehyde - Isoniazid - Lactic Acidosis - Etoh/Ethylene Glycol - Rhabdo/Renal Failure Salicylates Non-Anion Gap Acidosis: HARDUPS Hyperalimentation Acetazolamide - Renal Tubular Acidosis - Diarrhea - Uretero-Pelvic Shunt - Post- Hypocapnia - Spironolactone Anion gap = Na + (meq/l) [Cl - (meq/l) + HCO 3 - (meq/l)] Greater than 10 meq/l in mild cases and greater than 12 meq/l in moderate and severe cases Diabetic ketoacidosis is typically characterized by hyperglycemia over 250 mg/dl (14 mmol/l), a bicarbonate level less than 18 mmol/l, and a ph less than 7.30, with ketonemia and ketonuria.

7 Lab Results Case 1 Blood test, performed 2-month PTA were normal Blood Test WBC 13.8 X 10 9 /L (4-10 X 10 9 /L) Sodium 131 mmol/l ( mmol/l) Chloride 94 mmol/l ( mmol/l) Urea 20.3 mmol/l ( mmol/l) Creatinine 885 mmol/l (50-90 mmol/l) Estimated GFR 5.06 ml/min/1.73 m² (~85 in ages 60-70) Albumin 25 g/l (35-50 g/l) Urine Dipstick positive for protein, with a few RBC Microscopic examination shows fatty casts and few monomorphic RBC On US, both kidneys appear slightly larger and the kidneys parenchyma appear hyperechoic compared to the liver, suggestive of renal parenchymal disease Case 2 ph 7.18 ( ) Serum Bicarbonate 13.7 mmol/l (24-30 mmol/l) Arterial PaCO2 29 mmhg (35-45 mmhg) Arterial PaO2 53 mmhg ( mmhg) Arterial SaO2 87% (96-100%) Blood Glucose 25.5 mmol/l ( mmol/l) Serum Sodium 134 mmol/l ( mmol/l) Serum Chloride 95 mmol/l ( mmol/l) Serum Potassium 4.1 mmol/l ( mmol/l) Serum Creatinine 97 mmol/l ( mmol/l) Urinalysis positive for ketones