Whereas a high protein diet appears to have certain advantages including avoiding weight gain and maintaining a favorable glycemic index, its impact on kidney health is less clear. High dietary protein intake can cause intraglomerular hypertension, which may result in renal hyperfiltration, glomerular injury and proteinuria. In the studies with animal model feeding high protein diets, the increase in the glomerular filtration rate (GFR), a marker of hyperfiltration, was dose-dependent with the amount of protein diet as a maximal GFR increase of nearly 80%. It was also manifested in human data that high protein consumption increased estimated GFR compared to lower protein diets in RCTs. Although the exact mechanisms of protein-induced glomerular hyperfiltration have not been fully elucidated, it is thought to occur as an evolutionary feedback mechanism facilitating the excretion of increased amounts of protein-derived nitrogenous waste. Changes in endocrine mediators leading to vasodilation (e.g., glucagon and insulin-like growth factor I) and changes in neurohormonal responses within the kidney (i.e., tubuloglomerular feedback) have also been posited as underlying mechanisms to facilitate the increased excretion of nitrogenous waste. Although some instances of short-term glomerular hyperfiltration, like pregnancy, may not be associated with a decrease in kidney function, it is possible that prolonged, recurrent glomerular hyperfiltration induced by a high protein diet consumption may lead to kidney damage over time through multiple pathways. Experimental data have shown that incrementally higher levels of protein intake (i.e., 20%, 30%, and 45% of total energy content) caused an increase in pro-inflammatory gene expression in a dose-dependent manner, and long-term exposure to a high protein diet (i.e. 35% of energy intake) led to greater renal fibrosis and greater glomerulosclerosis. Hence, with long term daily or frequent high protein intake, de novo chronic kidney disease (CKD) may ensue, or the course of CKD may be accelerated. For the most part of long-term population studies, deterioration of renal function over time has been observed in the highest dietary protein intake group, especially among patients with renal insufficiency or comorbidities increasing the risk of renal disease such as hypertension and diabetes. Those with a solitary kidney are likely at risk as well. When compared to other sources of protein, animal protein is more likely associated with the risk of end-stage of renal disease. Metabolic derangement such as acidosis or hyperphosphatemia is also believed to be consequences of a high protein diet, especially from animal sources. Although low-carbohydrate and ketogenic diets have gained interest recently, basic characteristics of thsee kinds of diets are higher proportion of animal protein, which may cause renal injury in the long-term. Current dietary trends with high proportion of protein for weight reduction should be carefully practiced in those at high risks of kidney disease, and long-term studies based on large populations to better ascertain the impact of high protein intake are warranted.