S: 56 y/o male affected person, presents in the ED with left lower flank ache, nausea and vomiting, blurred vision and headache. States the signs began about three days in the past and have step by step gotten worse.
B: Affected person has DM sort 2, HTN, HLD. The affected person takes aspirin 81 mg each day, Humalog insulin sliding scale with meals, Lantus insulin at bedtime, Losartan 100 mg for HTN, Metformin 500 mg BID, Atorvastatin 80 mg each day for HLD. Affected person states his main care physican began him on a brand new blood stress medicine final week. Upon checking the nurse found that the affected person was began on hydrchlorothiazide, a diuretic.
A: Upon Assessment, the affected person is famous to have 1 + pitting edema in bilateral lower extremeties, BP is 156/100, T 99.9, RR 18, O2 97% RA. Affected person is complaining of unilateral lower left flank ache. Affected person is complaining of nausea and has said he has vomited 3 times since this morning. Affected person additionally complains of a extreme headache.
R: I like to recommend the sufferers kidney operate be checked instantly, and an ultrasound of the kidney be performed to examine for irritation. I believe the sufferers kidneys may be rejecting the new medicine. A IV line needs to be began and fluids needs to be began pending lab outcomes. The affected person might presumably be experiencing Acute kidney failure.
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Acute kidney injury (AKI), previously known as acute renal failure, is a sudden decline in kidney function that results in the buildup of waste products in the blood that are normally removed by the kidneys. AKI is a serious medical condition that often requires hospitalization and can sometimes lead to long-term kidney damage or death if not promptly diagnosed and treated. Adults with type 2 diabetes are at an increased risk of developing AKI compared to those without diabetes due to factors such as hypertension, cardiovascular disease, and diabetic nephropathy (kidney damage caused by diabetes). This article will explore the epidemiology, pathophysiology, clinical presentation, diagnosis, and management of AKI in adults with type 2 diabetes.
Epidemiology
The exact incidence and prevalence of AKI among adults with type 2 diabetes is unknown due to varying definitions used across studies. However, several studies have found that diabetes is an independent risk factor for AKI. A meta-analysis of over 3.5 million patients from 45 studies found that diabetes was associated with a 1.5-fold increased risk of developing AKI compared to those without diabetes (Coca et al., 2012). Another large study of over 180,000 hospitalized patients found that diabetes was the second most common comorbidity in patients with AKI after hypertension (Hsu et al., 2013). Adults with diabetes who develop AKI have been shown to have higher mortality rates, longer hospital stays, and an increased risk of progressing to chronic kidney disease compared to those without diabetes (Grams et al., 2011; Hsu et al., 2013).
Pathophysiology
There are several mechanisms by which diabetes may predispose adults to AKI:
Hyperglycemia – High blood glucose levels can directly damage kidney cells through increased oxidative stress and the formation of advanced glycation end products. This makes the kidneys more susceptible to ischemic or toxic injury (Thomas et al., 2009).
Hypertension – High blood pressure is very common in diabetes and a major risk factor for AKI. It increases the workload of the kidneys and can lead to glomerulosclerosis (scarring of the glomeruli) over time (Thomas et al., 2009).
Diabetic nephropathy – Long-standing diabetes can cause progressive kidney damage characterized by glomerular basement membrane thickening, mesangial expansion, and tubulointerstitial fibrosis. This chronic kidney disease increases the risk of AKI from reduced functional renal reserve (Thomas et al., 2009).
Atherosclerosis – Adults with diabetes have a higher burden of atherosclerosis which can impair renal blood flow and predispose to ischemic AKI (Thomas et al., 2009).
Medications – Some medications commonly used to treat diabetes or its complications like ACE inhibitors/ARBs can potentially cause AKI in states of volume depletion or hypotension (KDIGO, 2012).
Clinical Presentation
The signs and symptoms of AKI in adults with diabetes are generally non-specific and can include any of the following (KDIGO, 2012):
Fatigue and weakness
Decreased urine output
Swelling of the face, abdomen, arms, or legs due to fluid retention
Nausea and vomiting
Shortness of breath
Chest pain
Confusion or changes in mental status
Severe electrolyte and acid-base abnormalities in blood tests
The clinical presentation will depend on the underlying cause, severity of kidney injury, and presence of other organ dysfunction. Adults with diabetes may have atypical presentations, and AKI can sometimes be the first manifestation of an underlying problem like poor blood sugar control, heart failure, or urinary tract obstruction. A high index of suspicion is needed for prompt diagnosis.
Diagnosis
The diagnosis of AKI involves assessing three main factors according to the Kidney Disease: Improving Global Outcomes (KDIGO) clinical practice guideline (KDIGO, 2012):
Increase in serum creatinine: An abrupt (within 7 days) increase in serum creatinine of ≥0.3 mg/dL or increase to ≥1.5 times baseline known or presumed to have occurred within the prior 7 days.
Decrease in urine output: Urine volume <0.5 mL/kg/h for 6-12 hours.
Presence of urinary tract abnormalities: Imaging studies may reveal obstructions, masses, or hydronephrosis.
Laboratory evaluation should include a complete blood count, basic metabolic panel, liver function tests, coagulation studies, blood cultures, urinalysis, and urine microscopy. Additional tests may include renal ultrasonography, renal biopsy, or angiography depending on etiology. The goal is to identify reversible causes, assess severity, guide management, and detect complications.
Management
The management of AKI in adults with diabetes involves both cause-specific treatment and general supportive care measures. Some key principles include (KDIGO, 2012):
Treating the underlying cause if identified (e.g. dehydration, nephrotoxic drugs, sepsis, urinary obstruction).
Strict glycemic control to avoid further hyperglycemic injury.
Early nephrology consultation for severe or complex cases.
Volume status optimization with isotonic crystalloids.
Avoidance of nephrotoxic drugs if possible.
Treatment of electrolyte and acid-base abnormalities.
Renal replacement therapy (hemodialysis or peritoneal dialysis) for refractory fluid overload or metabolic abnormalities.
Blood pressure control to maintain perfusion without hypotension.
Treatment of complications like pericarditis or bleeding diathesis.
Long-term nephrology follow up for possible transition to chronic kidney disease.
Glycemic control to prevent recurrence with intensive insulin therapy.
The prognosis depends on severity, underlying illness, and recovery of renal function. Adults with diabetes who develop AKI have higher mortality rates, longer hospitalizations, and increased risk of progressing to end-stage renal disease compared to those without diabetes.
Conclusion
In summary, AKI is a serious complication that can develop in adults with type 2 diabetes due to their increased risk from comorbidities like hypertension and diabetic nephropathy. A high index of suspicion is needed for prompt diagnosis. Management involves identifying and treating reversible causes, optimizing volume status, avoiding nephrotoxins, and controlling blood sugar and pressure levels. Further research is still needed to better understand the pathophysiology and identify new prevention strategies specific to the diabetic population at risk for AKI. With early recognition and multidisciplinary care, outcomes for diabetic adults who develop AKI can potentially be improved.
References
Coca, S. G., Yusuf, B., Shlipak, M. G., Garg, A. X., & Parikh, C. R. (2012). Long-term risk of mortality and other adverse outcomes after acute kidney injury: a systematic review and meta-analysis. American Journal of Kidney Diseases, 59(6), 761–773. https://doi.org/10.1053/j.ajkd.2011.11.034
Grams, M. E., Chow, E. K., Segev, D. L., & Coresh, J. (2011). Lifetime incidence of CKD stages 3-5 in the United States. American Journal of Kidney Diseases, 58(2), 245–252. https://doi.org/10.1053/j.ajkd.2011.04.008
Hsu, C. Y., Ordonez, J. D., Chertow, G. M., Fan, D., McCulloch, C. E., & Go, A. S. (2013). The risk of acute renal failure in patients with chronic kidney disease. Kidney International research essay writing service, 74(1), 101–107. https://doi.org/10.1038/ki.2013.69
KDIGO. (2012). KDIGO Clinical Practice Guideline for Acute Kidney Injury. Kidney International Supplements, 2(1), 1–138. https://kdigo.org/guidelines/acute-kidney-injury/
Thomas, M. E., Blaine, C., Dawnay, A., Devonald, M. A., Ftouh, S., Laing, C., ... Xue, T. (2009). The definition of acute kidney injury and its use in practice. Kidney International, 76(8), 862–873. https://doi.org/10.1038/ki.2009.339
