Acute Kidney Injury and Chronic Kidney Disease Case Study: Azotemia vs. Uremia, Protein Restriction, Anemia and Left Ventricular Dysfunction

Case Study: Acute Kidney Injury and Chronic Kidney Disease (Will, 68)

Will is a 68-year-old man with hypertension who started dialysis for end-stage renal disease (ESRD) eight months ago. Before that, he had polyuria and nocturia, his hypertension became difficult to manage, and he lost his appetite, became weak and easily fatigued and developed ankle edema. His physician insisted on dialysis before uremic signs increased.

1. What is the difference between azotemia and uremia?
2. Two years ago, Will’s physician told him to decrease his protein intake, but he kept eating chicken, beef, pork or eggs daily. Why did his physician warn him about his diet?
3. Will’s weakness and fatigue are symptoms of anemia. Why is he anemic?
4. Why is left ventricular dysfunction a concern for his physician?

Original example for study purposes (about 580 words). Add citations from your pathophysiology textbook.

Azotemia Versus Uremia

Azotemia is a laboratory finding: an elevated level of nitrogenous waste products, mainly blood urea nitrogen (BUN) and creatinine, in the blood because the kidneys’ glomerular filtration rate (GFR) has fallen. A person can have azotemia without symptoms. Uremia is the clinical syndrome that develops when kidney failure becomes advanced and retained waste products and metabolic disturbances affect many body systems. Signs of uremia include nausea, vomiting, anorexia, fatigue, a metallic taste, itching, confusion or impaired concentration, peripheral neuropathy, bleeding tendencies, pericarditis and, in severe cases, seizures and coma. In short, azotemia is a laboratory abnormality, while uremia is a symptomatic, multisystem illness; Will’s anorexia, weakness and fatigue were early signs that he was moving toward uremia.

1. Why His Physician Warned Him About Protein

Protein is broken down into amino acids, and the nitrogen they contain is converted into urea, which must be excreted by the kidneys. When kidney function declines, a high-protein diet increases the amount of urea and other nitrogenous waste in the blood, worsening azotemia and accelerating uremic symptoms such as nausea and fatigue. High protein intake also increases the workload of the remaining nephrons through glomerular hyperfiltration, which can speed the progression of chronic kidney disease (CKD). Animal proteins such as beef, pork, chicken and eggs are also high in phosphorus, and failing kidneys cannot excrete phosphorus well, leading to hyperphosphatemia, which contributes to bone disease (CKD mineral and bone disorder) and vascular calcification. Many processed meats are also high in sodium, which worsens hypertension and fluid retention. Before dialysis, a moderate, controlled protein intake was recommended to slow progression and reduce symptoms. (Note: once patients begin dialysis, protein needs usually increase because dialysis removes amino acids, so Will’s diet should now be guided by a renal dietitian.)

2. Why Will Is Anemic

Will’s anemia is mainly caused by decreased production of erythropoietin. Erythropoietin is a hormone made primarily by peritubular cells in the kidney in response to low oxygen levels, and it stimulates the bone marrow to produce red blood cells. As functioning kidney tissue is lost in CKD, erythropoietin production falls, so fewer red blood cells are produced, resulting in a normocytic, normochromic anemia. Other contributing factors include a shortened red blood cell life span caused by uremic toxins, iron deficiency (from poor intake, reduced absorption and blood loss during dialysis and frequent blood draws), folate or vitamin B12 deficiency and uremia-related bleeding tendencies. The anemia reduces oxygen delivery to tissues, which explains his weakness and fatigue. It is typically treated with erythropoiesis-stimulating agents and iron supplementation.

3. Why Left Ventricular Dysfunction Is a Concern

Cardiovascular disease is the leading cause of death in people with CKD and ESRD, and Will has several risk factors for left ventricular dysfunction. Long-standing hypertension, which became harder to control as his kidney function declined, increases afterload, forcing the left ventricle to pump against high pressure and leading to left ventricular hypertrophy (LVH). Fluid overload from sodium and water retention, seen in his ankle edema, increases preload and stretches the ventricle. Anemia forces the heart to increase cardiac output to deliver enough oxygen, adding further workload. CKD also promotes vascular calcification and arterial stiffness through calcium-phosphate imbalance, and uremic toxins and inflammation can damage the heart muscle. Over time, LVH can progress to diastolic and systolic dysfunction, heart failure, arrhythmias and sudden cardiac death. His physician must therefore carefully manage blood pressure, fluid removal during dialysis, anemia and mineral balance to protect his heart.

References

[Your pathophysiology textbook chapter on renal disorders, in APA format.]

Kidney Disease: Improving Global Outcomes (KDIGO) CKD Work Group. (2024). KDIGO 2024 clinical practice guideline for the evaluation and management of chronic kidney disease. Kidney International, 105(4S), S117–S314. https://doi.org/10.1016/j.kint.2023.10.018

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