CHAPTER 22 Renal Disorders 555
occur that cause paresthesias and burning in the legs and feet. Restless leg syndrome can occur, which is characterized by ill-defined sensations in the legs that are relieved by movement. Hiccups, abdominal cramps, and muscular twitching can occur. Gastri- tis, peptic ulcer disease, constipation, and mucosal ulcerations of the GI tract often occur. Uremic fetor, a urine-like odor on the breath, from the breakdown of urea to ammonia in saliva, can occur. Anorexia, nausea, and vomiting due to the retention of toxins is common. Pruritus is very common in CKD and hyper- pigmentation of the skin can occur due to retained metabolites and toxins. Glucose metabolism is impaired in CKD. Serum glucose and serum insulin levels can be elevated. In women with CKD, estrogen levels are low and men- strual abnormalities, infertility, and inability to carry pregnancies to term are common. Pregnancy can worsen kidney function in women with CKD and spon- taneous abortion is common. Men with CKD have diminished testosterone levels with decreased sperm count and sexual dysfunction. Diagnosis A CBC with differential, serum electrolytes, serum creatinine, total albumin, BUN, and urinalysis will demonstrate abnormalities of renal failure. Normo- chromic normocytic anemia is seen in CKD caused by lack of erythropoietin. Sodium, potassium, bicar- bonate, and other electrolytes will be elevated in the bloodstream. Hyperkalemia may cause cardiac dys- rhythmias, requiring electrocardiogram (ECG) mon- itoring. BUN and creatinine levels will be elevated because all nitrogenous wastes are accumulating in the bloodstream. When 50% of nephrons are dysfunc- tional, serum creatinine rises to approximately double the normal blood level. Patients will have hypoalbu- minemia caused by glomerular damage, which causes loss of protein into the urine. Proteinuria is a classic sign of renal dysfunction. Serum calcium and vita- min D levels are low and PTH levels are elevated. CKD causes secondary hyperparathyroidism, which leads to decreased bone density and fragility. Hyper- phosphatemia occurs because of hypocalcemia. Renal ultrasound and other imaging studies may be indi- cated. Other more disease-specific blood tests may be done according to etiology of renal failure. Urinalysis will likely show protein, RBCs, and WBCs, as these will all be lost in the urine. A 24-hour urine collection for protein and creatinine clearance will show excessive loss of protein. However, a single urine specimen can be used to calculate the protein-to- creatinine ratio, which allows reliable approximation of total 24-hour urinary protein excretion. The calcu- lation usually shows protein loss greater than 2 grams in the urine. Noninvasive renal imaging studies such as x-ray, ultrasound, CT, and MRI can show any intrarenal
masses, cysts, or calcium stones. IV contrast-enhanced studies should be avoided in renal failure. Treatment Fluid and electrolyte management is critical to the management of patients with CKD. Excess fluid can lead to heart failure and pulmonary edema. Salt restriction and loop diuretics (e.g., furosemide) are commonly necessary. HTN due to renin hypersecre- tion and anemia due to lack of erythropoietin develop early during the course of CKD. Blood pressure man- agement is indicated with cautious use of ACE inhib- itors or angiotensin receptor blockers. These agents can raise potassium; therefore, potassium levels must be monitored. Erythropoietin-stimulating medica- tions (e.g., epoetin alfa) are also usually administered. Iron supplements are needed when erythropoietin- stimulating agents are administered because of active RBC production. Hyperphosphatemia can be treated with dietary phosphate binders (e.g., PhosLo) and dietary phosphate restriction. Dysfunctioning kidneys do not produce portions of vitamin D; there- fore, calcium is not absorbed from the GI tract. This causes hypocalcemia, which stimulates parathyroid hyperfunction. Hypocalcemia can be treated with cal- cium supplements that contain vitamin D. Calcitriol is synthetic vitamin D. Calcimimetic agents are used to counteract the hyperparathyroid activity. Hyper- kalemia can be reduced with potassium-lowering agents, such as patiromer or sodium polystyrene, and low-potassium diet. Dietary salt substitutes should not be used as these are potassium-based. Intracta- ble hyperkalemia is an indication to start dialysis in a CKD patient. Metabolic acidosis can be reversed with sodium bicarbonate administration. Blood glucose levels and serum insulin levels can become abnor- mal. Certain antidiabetic medications such as met- formin and sulfonylureas are contraindicated in CKD. However, the gliflozin antidiabetes medications that inhibit sodium-glucose transport in the nephron (also called SGLT2 inhibitors) are considered renal-protec- tive. SGLT2 inhibitors (e.g., dapagliflozin) can lower blood glucose and stabilize GFR in kidney disease. They have been shown to decrease cellular injury in the proximal tubules of the nephrons in patients with CKD. These medications are currently under study to see if they confer kidney protection in other renal diseases (Wheeler et al., 2020). To counteract pruri- tus, topical corticosteroids and antihistamines can be used (see Patho-Pharm Connection). Complications CKD can progress to ESRD. In ESRD, there are body- wide adverse effects (see Fig. 22-14). As the disease progresses and other systems are involved, the patient may develop respiratory compromise related to fluid overload, HTN, and uremic coma. In ESRD, treatment options include hemodialysis (in clinical setting or
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